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Free Radicals Nitric Oxide and Inflammation Molecular
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FREE RADICALS, NITRIC OXIDE, AND INFLAMMATION:
MOLECULAR, BIOCHEMICAL, AND CLINICAL ASPECTS
NATO Science Series

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 Free Radicals, Nitric Oxide, and
Inflammation: Molecular,
Biochemical, and Clinical Aspects

Edited by

Aldo Tomasi
Department of Biomedical Science, School of Medicine,
University of Modena, Italy

Tomris Ozben
Department of Biochemistry, School of Medicine,
Akdeniz University, Antalya, Turkey

and

Vladimir P. Skulachev
A.N. Belozersky Institute of Physico-Chemical Biology,
Moscow State University, Russia

/OS
Press

Ohmsha

Amsterdam • Berlin • Oxford • Tokyo • Washington, DC

Published in cooperation with NATO Scientific Affairs Division

Proceedings of the NATO Advanced Study Institute on
Free Radicals, Nitric Oxide, and Inflammation: Molecular, Biochemical, and Clinical Aspects
23 September - 4 October 2001
Antalya, Turkey

© 2003, IOS Press

All rights reserved. No part of this book may be reproduced, stored in a retrieval system, or transmitted,
in any form or by any means, without prior written permission from the publisher.

ISBN 1 58603 243 7 (IOS Press)

ISBN 4 274 90504 7 C3045 (Ohmsha)
Library of Congress Control Number: 2002104884

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 Foreword
Inflammation is the local response of a complex organism to an injury that serves as a
mechanism initiating the elimination of noxious agents and of damaged tissues. It is now
well understood that damaging mechanisms at the basis of very common human
pathologies, such as atherosclerosis, neurodegenerative disesases, and cancer, i.e. the most
common human pathologies, are driven by the inflammatory process.
Free radicals, and the very special free radical nitric oxide, are playing a relevant role
in the pathogenesis of inflammation. The book reports topics taught and discussed during
the NATO Advanced Study Institute course held in Antalya, September 23–October 4
2001.
The initial chapters introduce to the general knowledge necessary to understand the
inflammatory process and the role played of free radical and oxidative stress. The interplay
between inflammatory molecules and cell signalling is also dealt with in depth. A second
part is dedicated to nitric oxide, redox regulation and antioxidant function in inflammation.
The final chapters are devoted to diseases where inflammation plays the dominant role:
septic shock, end-stage renal disease, neurodegenerative, ischemic and lung diseases.
This book, while not covering the whole gamut of the massive literature on
inflammation and human diseases, gives an updated and concise view on the major issues
concerning the pivotal role of inflammation in so many different human pathologies. At the
same time it gives directions for future paths of research leading to a control of the
pathologic process.

Aldo Tomasi, Tomris Ozben and Vladimir Skulachev,

Editors
This page intentionally left blank
 Contents
Foreword v

Alternative Functions of Mitochondria, V.P. Skulachev 1

The Enzymatic Systems in the Regulation of Free Radical Lipid Peroxidation,
V.Z. Lankin 8
Flavanols and Procyanidins as Modulators of Oxidation in vitro and in vivo,
• C.G. Fraga and C.I. Keen 24
Estimation of Oxidative and Lipids Peroxidation DNA Adduct in Urine and DNA.
Methodological Aspects and Application in Molecular Epidemiology,
H.E. Poulsen 34
Oxidative and Nitrosative Stress Mediated by Cyclosporine A in Endothelial Cells,
J. Navarro-Antolin and S. Lamas 39
Early Signaling with Iron and Copper in Ischemic Preconditioning of the Heart,
B. Vaisman, E. Berenshtein, C. Goldberg-Langerman, N. Kitrossky,
A.M. Konijn and M. Chevion 46
Multiple Mechanisms Regulating Endothelial Nitric Oxide Synthase,
A. W. Wyatt and G.E. Mann 60
Nitric Oxide. Its Generation, Reactions and Role in Physiology, T.M. Millar,
J.M. Kanczler, T. Bodamyali, C. Stevens and D.R. Blake 71
Redox-Regulated Glutathionylation of Transcription Factors: A Regulatory Mode
for Gene Expression, E. Pineda-Molina and S. Lamas 89
Sulphur-Containing Amino Acids, Glutathione and the Modulation of
Inflammation, F. Santangelo 102
Molecular Events of the Inflammation Process that are Affected by a-Tocopherol.
Antioxidants and Gene Expression in the Process of Inflammation and
Wound Repair, A. Azzi, J.-M. Zingg, T. Visarius and R. Ricciarelli 112
Redox Regulation, Cytokine, and Nitric Oxide in Inflammation, A. Tomasi,
S. Bergamini, C. Rota and A. lannone 119
Non-Traditional Cardiovascular Disease Risk Factors and Arterial Inflammatory
Response in End-Stage Renal Disease, T. Ozben 132
Significance of Reactive Oxygen Species for Neuronal Function,
A.A.Boldyrev 153
Protein Aggregates and the Development of Neurodegenerative Diseases,
A. Stolzing and T. Grune 170
Inflammatory Response of the Brain Following Cerebral Ischemia, T. Ozben 182
Carnosine as Natural Antioxidant and Neuroprotector: Biological Functions and
Possible Clinical Use, A.A. Boldyrev 202
Atherosclerosis as a Free Radical Pathology and Antioxidative Therapy of this Disease,
V.Z. Lankin and A.K. Tikhaze 218
H2O2 Sensors of Lungs and Blood Vessels and their Role in the Antioxidant Defense
of the Body, V.P. Skulachev 232
Oxidative Lung Injury, F.J. Kelly 237
Proper Design of Human Intervention Studies, Power Calculations, H.E. Poulsen 252

Author Index 255

This page intentionally left blank
Free Radicals, Nitric Oxide and Inflammation:
Molecular, Biochemical, and Clinical Aspects
A. Tomasi et al. (Eds.)
IOS Press, 2003

Alternative Functions of Mitochondria

Vladimir P. Skulachev
Department of Bioenergetics, A.N. Belozersky Institute of Physico-Chemical Biology,
Moscow State University, Moscow 119899, Russia
E-mail: [email protected]

Abstract: Mitochondria are known to be multifuctional intracellular organelles.

They carry out (i) energy conservation in forms of protonic potential and
ATP, (ii) thermoregulatory energy dissipation as heat, (iii) production of useful
substances, (iv) decomposition of harmful substances, and (v) regulation of
intracellular processes. It is suggested that mitochondria are equipped by a
mechanism of self-elimination ("mitoptosis") responsible for purification of
mitochondrial population from unwanted organelles (e.g., ROS-overproducing
mitochondria). Massive mitoptosis is assumed to induce apoptosis due to release of
the cell death proteins normally hidden in the intermembrane space of mitochondria.
In this way tissues are purified from ROS-overproducing and other unwanted cells.

1. Energy conservation

1.1 Phosphorylating respiration

The respiration-coupled energy conservation in form of ATP is usually the most important
mitochondrial function. In the aerobic cell, phosphorylating respiration is responsible, as a
rule, for production of 90-95 % of the total ATP amount, the rest being synthesized by
glycolytic phosphorylation. All the ATP synthesized from ADP and inorganic phosphate is
hydrolyzed back to ADP and phosphate to support the energy-consuming processes in the
same cell. The adult human forms and decomposes as much as about 40 kg ATP per day [1].
In mitochondria, more than 90 % of the respiratory phosphorylation is catalyzed by
the H+-ATP-synthase, an enzyme converting the respiratory chain-produced electro-
chemical H+ potential difference into ATP [1–4]. Very small (but sometimes
essential) portion of the respiratory energy is converted to GTP by succinate thiokinase [4].
Both respiratory chain enzymes (Complexes I, III and IV), catalyzing electron transfer from
NAD(P)H to 62, and H+-ATP-synthase are localized in the inner mitochondrial membrane.
The great majority of the formed ATP molecules is exported from mitochondria by the
ATP/ADP antiporter in exchange for extramitochondrial ADP (eqs. 1-3).
2 V.P. Skulachev /Alternative Functions of Mitochondria

ATP/ADP-antiporter
ADPout + ATPin ---------- > ADP,n + ATPout (3)

1.2 Non-phosphorylating energy-conserving respiration

The respiration-produced can be utilized by mitochondria not only to form ATP but
also to support some other energy-consuming processes namely reverse electron transfer in
the respiratory chain and uphill transport of certain solutes from cytosol to the
mitochondrial matrix.
Two reactions of the reverse electron transfer are of physiological significance. 1
mean (i) oxidation of succinate (redox potential, +0.03 V) by NAD + (redox potential, -0.32
V) and (ii) oxidation of NADH by NADPH responsible for maintenance of
[NADPH]/NADP+]>> [NADH]/[NAD+] in spite of the fact that redox potential of the
NADPH/NADH* pair is almost equal to that of NADH/NAD* pair. The former process
includes a reversal of NADH-CoQ reductase (Complex 1 of the respiratory chain). Usually
it operates as a generator catalysing the downhill electron transfer from NADH to
CoQ. However, when NAD+ is reduced by succinate, the same complex acts as a
consumer carrying out the uphill transfer of electrons from CoQHa to NAD+ [5].
Reduction of NADP+ by NADH is catalysed by H*-transhydrogenase, a
consumer competent in the H" transfer between two nicotinamide adenine nucleotide in a
-linked fashion. As a source of, respiration or ATP hydrolysis can be used [5],
The same energy sources are employed to create gradients of solutes between cytosol
and mitochondrial matrix. For instance, mitochondria accumulate Ca2* by means of
electrophoretic Ca2 uniporter.
ATP/ADP antiporter catalyzes transmembrane exchange of ADP3- for ATP4-. This
results in import of ADP and export of ATP at the expense of the respiration energy.

1.3 The long distance power transmission

Translated from Greek, the word "mitochondrion" means "thread-grain". This term was
introduced many years ago by cytologists who used the light microscope. The first students
of mitochondria always indicated that these organelles may exist in two basic forms:
(1) filamentous and (2) spherical or ellipsoid.
By applying the fluorescent cation method, it was revealed that a filamentous
mitochondria may represent an electrically united system operating as intracellular electric
cables. A local damage of such a filament by very narrow (0.5 in diameter) laser beam
was shown to cause efflux of the cation and, hence, the fluorescence decreases in the entire
50 mitochondrial filament in a human fibroblast cell.
Later the same approach was applied to study heart muscle mitochondria that
represent mainly spherical bodies. It was found that these organelles form electrically
conductive intermitochondrial contacts. As a result, heart mitochondria can be united to
clusters composed of tens spherical organelles (we coined them Streptio mitochondriale).
Both mitochondrial filaments and clusters were assumed to be used by the cell to transmit
inside the cell [4–6].

2. Energy dissipation

Almost all the energy conserved in form of ATP releases as heat when the ATP-dependent
functions of organism are performed. Thus, then the ambient temperature lowers, a man or
 V.P. Skulachev /Alternative Functions of Mitochondria 3

a warm-blooded animal can increase their functional activity and produce in this way
additional heat to keep constant the body temperature. This is the case when muscle
contractions are activated by the cold (so-called shivering thermogenesis). However, such a
mechanism is hardly optimal since here the main goal of thermoregulation (to make
physiological functions temperature-independent) is, in fact, not realized. Moreover,
shivering thermogenesis is rather complicated process requiring the H+-ATP-synthase-
produced ATP to be transported from mitochondria to cytosol and hydrolyzed by
actomyosin. Then the products (ADP and phosphate) should be transported in opposite
direction i.e. from cytosol to mitochondria. It is not surprising, therefore, that during cold
adaptation, the shivering thermogenesis is replaced by another mechanism which represents
much simpler way from respiration to heat and does not require the main (contractile)
function of muscle to be activated at cooling. The mechanism in question is
thermoregulatory uncoupling of respiration and phosphorylation.
Uncoupling results in dissipation of the respiratory chain-produced due to
increased H+ conductance of the inner mitochondrial membrane. Thus energy released by
respiration is immediately dissipated as heat without formation and hydrolysis of ATP.
Non-esterified fatty acids proved to be compounds mediating the thermoregulatory
uncoupling. They operate as protonophorous uncouplers with the help of special
uncoupling proteins (UCPs) or some mitochondrial antiporters i.e. the ATP/ADP antiporter
and aspartate/glutamate antiporter [1–5].

3. Synthesis of useful compounds

Both energy conservating and dissipating functions described above appear to be

alternative to the functions dealing with conversion of substances rather than energy.
Formally speaking, the respiration-linked substance interconversions might be carried out
by the same respiratory chain which is involved in the energy-linked functions. Sometimes
this really happens. However, if it were always the case, these functions would be tightly
coupled to the ATP synthesis and, hence, would be dependent upon the ADP availability.
Such a restriction is hardly desirable for the cell. This is why the metabolic functions of
respiration are catalyzed, at least in some cases, by non-coupled respiratory enzymes that
transfer electrons with no generated. For instance, some steps of the steroid hormone
syntheses in adrenal cortex mitochondria are mediated by special non-coupled respiratory
chain including a NADPH-oxidizing flavoprotein, the iron-sulphur protein adrenodoxin and
mitochondrial cytochrome P450. All of them are localized, like the energy-coupled
respiratory chain, in the inner mitochondrial membrane.
Biosyntheses of DNA, RNA and proteins in mitochondria can be another example of
constructive metabolic function of these organelles. It certainly requires ATP and therefore is
alternative to energy supply for extramitochondrial ATP-consuming processes [5].

4. Removal of unwanted compounds

Such a function may be exemplified by the urea synthesis from NHs. This ATP-consuming
process is localized in matrix of liver mitochondria. Like other intramitochondrial
biosyntheses, it is alternative to the ATP export from mitochondria to cytosol.
Oxidation of lactate after heavy muscle work seems to be another example of
mitochondrial function dealing with removal of a harmful compound responsible for
dangerous acidosis of the tissue. It was found that the ATP formation coupled to lactate
4 V.P. Skulachev /Alternative Functions of Mitochondria

oxidation by skeletal muscle mitochondria is smaller than that coupled to oxidation of any
other NADMinked substrate. This phenomenon was due to co-operation of non-coupled
and coupled respiratory chains.
Mitochondria can take part in antioxidant defence of the cell by maintaining low
intracellular oxygen concentration. In fact, this may be regarded as removal of an excess of
O2. Under resting conditions, this process seems to be carried out by partially uncoupled or
non-coupled respiration [5].

5. Mitochondria and reactive oxygen species

5.1 Mild uncoupling

Parallel with normal (enzymatic) four electron reduction of O2 to H2O by cytochrome

oxidase, non-enzymatic one electron reduction of O2 to superoxide (O2) takes place in
mitochondria. This "parasitic" chemical reaction appears to be inevitable since the initial
and middle steps of the respiratory chain contain very reactive electron carriers of negative
redox potential (e.g., chemically component in the one electron reduction of oxygen).
Besides non-enzymatic O2 generation, O2 can be enzymatically formed as a result
of the -consuming reverse electron transfer from succinate to O2. In fact, standard
redox potential of fumarate/succinate is slightly positive whereas that of O2/O2 is negative.
It was found that generated by succinate oxidation via Complexes III and IV can be
used to reduce O2 to O2 (eq. 4):

The process proved to be inhibited by even a small decrease ("mild

uncoupling") [5]. It was suggested that mild uncoupling is carried out by free fatty acids
operating as protonophores with the help of UCPs and ATP/ADP-antiporter [5].

5.2 Cytochrome c as an enzyme regenerating O2 from O2

Mild uncoupling seems to be a first line of the mitochondrial antioxidant defence which
prevents the O2 formation. If, nevertheless, some O2 is still formed, the next line of the
defence is actuated. This role can be performed by cytochrome c dissolved in the solution
occupying the intermembrane space of mitochondria. In fact, cytochrome c is competent in
oxidizing O2 back to O2
cyt. c3 + O2 cyt. c2+ + O2 (5)
3+ 2+
where cyt. c and cyt. c are for the oxidized and reduced cytochromes c, respectively.
Reduced cytochrome c formed by reaction (5) can then be oxidized by O2 via
cytochrome oxidase. In fact, the O2 oxidation by cytochrome c3+ represent the most
effective way to scavenge since O2 formed from O2 is converted back to 02. As for
the other reaction product, cyt. c2+, it can then be used to produce some in terminal
segment of the respiratory chain. We found, however, that the only the soluble, but not the
membrane-bound, cytochrome c is competent in superoxide oxidation. This means that
desorption of cytochrome c from the inner mitochondrial membrane can. in principle, be
 V.P. Skulachev /Alternative Functions of Mitochondria 5

regarded, besides an apoptosis-inducing events (see below, Section 8), also as activation of
an antioxidant system scavenging O2.

5.3 Other ROS scavengers

Besides cytochrome c, there are several other compounds operating as the ROS scavengers
but none of them can qualitatively convert O2 back to O2. Some scavengers are
irreversibly damaged when reacting with ROS, others can be regenerated from ROS-
oxidized form back to reduced form. For the water phase of the cell, reduced glutathione
and ascorbate are most important antioxidants whereas in membranes this function is
inherent, first of all, in tocopherol, carotenoids and CoQH2.
Important role is played by superoxide dismutase (SOD) converting the membrane-
impermeable superoxide anion (O2) to the membrane-permeable hydrogen peroxide
(H2O2). The latter can escape the cell to be diluted by extracellular medium. For unicellular
organisms, such a dilution is the final step of ROS detoxication. On the other hand, in
higher organisms hydrogen peroxide escaping the ROS-producing cell can be used an
alarm signal for its neighbours. Moreover, H2O2 is utilized inside the cell by glutathione
peroxidase. Oxidized glutathione formed is regenerated to the reduced glutathione by
glutathione reductase oxidizing NADPH. One more very important process of H2O2
removal is carried out by catalase which decomposes 2H2O2 to O2 and 2H2O [5].

5.4 Inhibition of aconitase by superoxide

Mitochondrial aconitase, enzyme catalyzing the first steps of the citric acid cycle, is known
to be reversibly inactivated by very low concentrations of O2 This should results in (i)
inhibition of supply of the respiratory chain by reducing equivalents and, hence, of the O2
formation, and (ii) accumulation of citrate, an excellent Fe2+ and Fe3+ chelator.
Autooxidable citrate3"-Fe2+ complex immediately reacts with O2. As a result, Fe2+ is
oxidized to Fe3+ , an effect preventing the production of OH', the most aggressive ROS,
which requires Fe2+ to be formed from H2O2 ("Fenton reaction"). The Fe3+ obtained
remains bound to citrate since its binding to citrate is much stronger than that of Fe2+ [5].
Interestingly, cytosolic aconitase was recently shown to function also as an iron
sensor. Earlier the cytosolic form of aconitase seemed to be an enzyme-"unemployed"
since the majority of other citric acid cycle enzymes are absent from cytosol. It was found,
however, that this enzyme plays a crucial role in regulating both the iron delivery to the cell
and iron storage [5].

6. Mitoptosis, programmed elimination of mitochondria

There is some indications that mitochondria possess a mechanism of self-elimination. This

function was ascribed to the so-called permeability transition pore (PTP). The PTP is a
rather large nonspecific channel located in the inner mitochondrial membrane. The PTP is
permeable for compounds of molecular mass < 1.5 kDa. The PTP is usually closed. A
current point of view is that PTP opening results from some modification and conformation
change of the ATP/ADP antiporter. Oxidation of Cys56 in the antiporter seems to convert it
to the PTP in a way that is catalyzed by another mitochondrial protein, cyclophilin. When
opened, the PTP makes impossible the performance of the main mitochondrial function,
i.e., coupling of respiration with ATP synthesis. This is due to the collapse of the
membrane potential and pH gradient across the inner mitochondrial membrane that mediate
respiratory phosphorylation. Membrane potential is also a driving force for import of
6 V. P. Skulachev / AIternative Functions of Mitochondria

cytoplasmic precursors of mitochondrial proteins. Moreover, it is strictly required for the

proper arrangement of mitochondrially-synthesized proteins in the inner membrane of the
mitochondrion. Thus, repair of the PTP-bearing mitochondrion ceases, and the organelle
perishes.
It is noteworthy that the above scheme of elimination of a mitochondrion does not
require any extramitochondrial proteins. It can be initiated by a signal originating from a
particular mitochondrion, such as reactive oxygen species (ROS) produced by the
mitochondrial respiratory chain. ROS seem to oxidize the crucial SH-group in the
ATP/ADP-antiporter, thereby actuating the elimination process. This is why one can
consider this effect as the programmed death of the mitochondrion (mitochondrial suicide).
For this event, I coined the word mitoptosis, by analogy with apoptosis, the programmed
death of the cell. I also suggested that the biological function of mitoptosis is the
purification of the intracellular population of mitochondria from those that became
dangerous for the cell because their ROS production exceeded their ROS scavenging
capacity. It seems very probable that antioxidant defense is not the only function of
mitoptosis. However, at least some alternative mitoptotic functions require ROS to be
formed as mediators of mitoptosis (for example, disappearance of mitochondria during the
maturation of the mammalian erythrocytes) [6–8].

7. Massive mitoptosis results in apoptosis

Opening of the PTP leads to an osmotic disbalance between the mitochondrial matrix and
cytosol, swelling of the matrix and, consequently, the loss of integrity of the outer
mitochondrial membrane, thus releasing the intermembrane proteins into the cytosol.
Among them, four proteins are of interest in this context: cytochrome c, apoptosis-inducing
factor (AIF), the second mitochondrial apoptosis-activating protein (Smac; also abbreviated
DIABLO), and procaspase 9. All these proteins are somehow involved in apoptosis.
In cytosol, cytochrome c combines with very high affinity with a cytosolic protein
called Apoptotic Protease-Activating Factor 1 (Apaf-1) and dATP. The complex, in turn,
combines with an inactive protease precursor, procaspase 9, to form the "apoptosome". As
a result, several procaspase 9 molecules are placed near each other, and they cleave each
other to form active caspases 9. When formed, caspase 9 attacks procaspase 3 and cleaves it
to form active caspase 3, a protease that hydrolyses certain enzymes occupying key
positions on the metabolic map. This causes cell death.
Considering these data, the following scenario of the final steps of the defense of a
tissue from mitochondrion-produced ROS seems to be most likely.
ROS induce PTP opening and, consequently, release of cytochrome c and other
proapoptotic proteins from mitochondria to the cytosol. If this occurs in a small fraction of
ROS-overproducing mitochondria, these mitochondria die. The cytosol concentrations of
proapoptotic proteins released from the dying mitochondria appear to be too low to induce
apoptosis. If, however, more and more mitochondria become ROS-overproduces, the
concentrations in question reach a level sufficient for the induction of apoptosis. This
results in purification of the tissue from the cells whose mitochondria produce too many
ROS.
In 1994, I postulated a scheme in which mitoptosis is an event preceding apoptosis
[9], In the same year, Newmeyer and coauthors published the first indication of a
requirement of mitochondria for apoptosis [10]. And quite recently, Tolkovsky and her
coworkers presented direct proof of the mitoptosis concept [11,12]. In the first set of
experiments, axotomized sympathetic neurons deprived of neuron grow factor were
studied. It was found that such neurons died within a few davs. showing cytochrome c
 V.P. Skulachev /Alternative Functions of Mitochondria 1

release and order typical features of apoptosis. However, the cells survive if a pan-caspase
inhibitor Boc-Asp (O-methyl)-CH2F (BAF) was added a day after the growth factor
deprivation. The cell survival was due to that the mitochondrion-linked apoptotic cascade
was interrupted downstream of the mitochondria. Electron microscopy showed that in such
cells all the mitochondria disappear within 3 days after the BAF addition. Later, the same
group reported that a similar effect could be shown using such classical experimental
models of apoptosis as HeLa cells treated with staurosporin. Again, addition of BAF to the
staurosporin-treated cells resulted in that (i) the cells lived longer and (ii) mitochondria
disappeared in the time scale of days. This was shown to be accompanied by disappearance
of mitochondrial DNA and as well as the cytochrome oxidase subunit IV encoded by
nuclear DNA. On the other hand, nuclear DNA, Golgi apparatus, endoplasmic reticulum,
centrioles, microtubules, and plasma membrane remained undamaged. Mitoptosis was
prevented by overexpression of antiapoptotic protein Bcl-2, which is known to affect
mitochondria upstream from the cytochrome c release.
Apparently, disappearance of mitochondria in the apoptotic cells without BAF could
not be seen since the cells die too fast to reveal mitoptosis and subsequent autophagia of
dead mitochondria. On the other hand, inhibition of apoptosis at a post-mitochondrial step
prevented fast death of the cells so there was time for mitoptosis to be completed [6,7].

References

[1] V.P. Skulachev, Membrane Bioenergetics, Springer, 1988.

[2] P. Mitchell, Chemiosmotic Coupling in Oxidative and Photosynthetic Phosphorylation, Biol. Rev. 41
(1966), 445-502.
[3] M. Saraste, Oxidative Phosphorylation at the fin de siecle. Science 283 (1999), 1488-1493.
[4] V.P. Skulachev, Energy transduction mechanisms (animals and plants). In: J.F. Hoffman and J.D.
Jamieson, eds., Handbook of Physiology, Amer. Physiol. Soc. Publ., New York, 1997, pp. 75–116.
[5] V.P. Skulachev, Mitochondrial physiology and pathology; concepts of programmed death of
organelles, cells and organisms. Mol. Asp. Med. 20 (1999), 139–184.
[6] V.P. Skulachev, Mitochondrial filaments and clusters as intracellular power-transmitting cables.
Trends Biochem. Sci. 26 (2001), 23–29.
[7] V.P. Skulachev, The programmed death phenomena, aging, and the Samurai law of biology. Exp.
Gerontol. 36 (2001), 995–1024.
[8] V.P. Skulachev, The programmed death phenomena: from organelle to organism. Ann. N.Y. Acad.
Sci. 959 (2002), 214–237.
[9] V.P. Skulachev, Lowering of intracellular O2 concentration as a special function of respiratory
systems of cells. Biochemistry (Moscow) 59 (1994), 1433-1434.
[10] D.D. Newmeyer, D.M. Farschon, and J.C. Reed, Cell-free apoptosis in Xenopus egg extracts:
inhibition by Bcl-2 and requirement for an organelle fraction enriched in mitochodria. Cell 79
(1994), 353-364.
[II] G.C. Fletcher, L. Xue, S.K. Passingham, and A.M. Tolkovsky, Death commitment point is advanced
by axotomy in sympathetic neurons. J. Cell Biol. 150 (2000), 741–754.
[12] L. Xue, G.C. Fletcher, and A.M.Tolkovsky, Mitochondria are selectively eliminated from eukaryotic
cells after blockade of caspases during apoptosis. Current Biol. 11 (2001), 361–365.
 Free Radicals, Nitric Oxide and Inflammation:
Molecular, Biochemical, and Clinical Aspects
A. Tomasi et ai (Eds.)
IOS Press, 2003

The Enzymatic Systems in the Regulation of

Free Radical Lipid Peroxidation
Vadim Z. Lankin
Cardiology Research Complex, 3-rd Cherepkovskaya 15 A, 121552 Moscow, Russia
E-mail: [email protected]

Abstract: Reviewing the data available in the literature and their own findings, the
author consider the role of enzymatic mechanisms in the regulation of lipid
peroxidation in the living cells. The paper provides a good evidence that
phospholipase A2 hydrolysis for reduction of hydroperoxy-derivatives of
unsaturated phospholipids by non-selenic glutathione S-transferase is not obligatory
moreover glutathione S-transferase may be inhibited by the products of
phospholipase A2 hydrolysis — by free unsaturated fatty acids. On the other hand,
Se-contained glutathione peroxidase is capable of reducing unsaturated
hydroperoxy-acyls of membrane phospholipids only if the phospholipids have been
hydrolyzed by phospholipase A2 and this enzyme is not inhibited in the presence of
free fatty acids. It can be suggested from the results that in normal conditions
glutathione S-transferase catalyzes direct reduction of oxidized membrane
phospholipid acyls, but during pathological stations, when the products of
phospholipase-mediated hydrolysis are accumulated (such as tissue ischaemia), the
major role in lipoperoxides detoxification in the cells belongs to Se-containing
glutathione peroxidase. In addition the accumulation of primary products
(hydroperoxy- and hydroxy-derivatives) of polyunsaturated acyl oxidative
metabolism in the phospholipid membranes induced the changes in the membrane
fluidity, that were opposite to those observed upon cholesterol incorporation into
membranes. It was found that antioxidative enzymes such as superoxide dismutase
and glutathione peroxidase may play a leading role in the prevention of the pancreas
ß-cells in vivo from reactive oxygen species injury in alloxan-treated rats.

Reactive oxygen species (ROS) represent groups of oxygen-containing molecules in

different states of oxido-reduction and electronic excitation, as well as compounds of
oxygen with hydrogen, chlorine and nitrogen, such as superoxide anion-radical (O2*),
hydrogen peroxide (H2O2), hydroxyl radical (HO), hypochlorous acid (HOC1), nitricoxide
(NO) and peroxynitrite (ONOO) [1]. Some of ROS such as O2, HO and NO are free
radicals. Free radicals can be defined as any species that contain one unpaired electron
(symbolized by *) on the external orbital of molecule [1]. Free radicals are highly reactive
species and can react with different organic compounds of the living cell — unsaturated
lipids of biomembranes, proteins and nucleic acids and cause the oxidative damage of its
molecules [1–3]. It was known to chemistry that hydroxyl radical (HO) is the most reactive
radical [1]. Endogenous prooxidants such as H2O2, HOC1 and ONOO can be regarded as
potentially dangerous molecules for living cells so far as they are degraded with HO*
formation:
 V.Z. Lankin / The Enzymatic Systems in the Regulation of Free Radical Lipid Peroxidation 9

H2O2 + Fe2+ -> HO + OH + Fe3+ (Fenton reaction);

Fe2+
H2O2 + O2 > HO + OH + O2 (Haber-Weiss reaction);

HOC1 + O2- -> HO + Cr + O2;

H+
NO + O2 > ONOO => ONOOH -» HO + NO2.
The different ROS, free radicals and endogenous inductors of free radical oxidation
which are frequently found in nature are presented in Figure 1.

Figure 1. The main forms of reactive oxygen species, free radicals and endogenous inductors of free radical
oxidation which are widely distributed in the living cells.

In the living cells the HO* preferentially attacks polyunsaturated fatty acids (PUFA)
of membrane phospholipids and it abstracts an atom of hydrogen from one of carbon atoms
in the side chain PUFA and combines with it to form water [1]:
LH + HO -> H2O + L.
Lipid carbon-centered alkil radical (L) is to combine with molecule of oxygen with
peroxyl radical (LO 2 ) formation:
L+O2-»LO2.
Peroxyl radical is reactive to attack another PUFA acyls, abstracting hydrogen. In this
reaction lipid hydroperoxide (LOOH) is formed and a new lipid alkil radical is generated
[1,2]:
LO 2 +LH-»LOOH + L.
The LOOH is very labile and can be decomposed with formation of secondary lipid
alkoxyl radical which interact with PUFA and over again generate lipid carbon-centered
radical:
10 V.Z. Lankin / The Enzymatic Systems in the Regulation of Free Radical Lipid Peroxidation

LOOM -> OFT +LO

The decomposition of LOOH can also yield a number of highly cytotoxic products,
malondialdehyde and 4-hydroxynonenal are most unpleasant among them. Lipid radicals
and cytotoxic aldehydes can also cause severe damage of membrane proteins, inactivating
receptors and membrane-bound enzymes [1–3].
There are three initiation mechanisms for the free radical lipid peroxidation in the
living cells. At the first lipoperoxidation in the body can be induced by non-enzymatic
mechanism. In this processes different physical factors such as ionizating irradiation or UV
radiation as well as action of some chemical toxicants including air pollutants, pesticides
and herbicides from food and drinking water may act as a initiating factors.
The second initiation way for the lipoperoxidation in the organism can be defined as
semi -enzymatic or quasi-enzymatic. During this mechanism the O2 radicals are generated
by enzymes including NAD(P)H-dependent oxidases of mitochondrial and microsomal
electron transport chaines, NADPH-dependent oxidase of phagocytes, xanthine oxidase and
other flavine oxidases. After the HO formation the oxidation process develops in non-
enzymatic way.
Finally the lipoperoxidation process can be fully enzymatic and this is carried out by
heme-containing cyclooxigenases (prostaglandin-, tromboxan- and prostacyclin-synthases)
or ferrous ione-containing lipoxygenases which are oxidized arachidonic acid and another
PUFA by means of free radical mechanism [4.5] as can be seen in Figure 2.

Figure 2. Free radical mechanism of enzymatic arachidonate oxidation by cyclooxigenase or lipoxygenase.

 V.Z. Lankin / The Enzymatic Systems in the Regulation of Free Radical Lipid Peroxidation 11

In particular the C-15 animal lipoxygenase may oxidize unsaturated acyls of

membrane phospholipids [6,7] (Figure 3) and this process plays the leading role in the
internal cell membranes decomposition during maturation of reticulocyte to erythrocyte [6].

Figure 3. The oxidation of various native membrane preparations by animal (rabbit reticulocyte) C-15
lipoxygenase: (1), erythrocyte ghosts; (2), liver microsomes; (3), liver mitochondria.

In addition lipohydroperoxides formed by C-15 lipoxygenase after its homolysis can

give rise to lipid alkoxyl radicals which induce cooxidation of other unsaturated lipids such
as p-carotene [8] (Figure 4).

wavelength, nm

Figure 4. The cooxidation of P-carotene (.=450 nm) by secondary lipid free radicals which formed during
arachidonic acid peroxidation ( = 2 3 3 nm) by animal (rabbit reticulocyte) C-15 lipoxygenase in the water
dispersions.

At present there are can be no doubt that investigations into the enzymatic regulation
of free radical reactions in the body is of high priority. A number of enzymes called as
"antioxidative enzymes" may act as effective antioxidants in vivo. It is known that
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 GENEALOGICAL GUIDE TO THE EARLY SETTELRS OF
AMERICA. 177 ELLMES: — Rbod'olphus EUmes, of Sci'tuate, came in
the "Planter," 1635, aged 15, married 1644, Catharine, daughter of
Jolm W'hitcomib, 'ha'd Sarah, 1645; Mary, 1648; Joanna, 1651;
Hannah, 1653, John, 1655; Joseph, 1658; Waitstill, 1661; Jonathan,
1663; and Rhodolphus, 1668. References: — ^Deane's Hist, of
Scituate, Mass., 266. ELLMiS. Eaton's Hist, of Thomaston, Me., 20i9.
ELLSWORTH:— Jeremiaih Ellsworth, of Rowley, 1650, marrie'd 1657,
Mary, widow of Hugh Smith, died 1704. JosiAH Ellsworth, ai Windsor,
married 1654, Elizabeth, daug'hter of Thomas Holcomb, 'had Josiah,
16 J5; Elizaibetlh, 1657; Mary, 1660; Martha, 1662; Thomas, 1665;
Jonathan, 1669; John, 1671; Job, 1674; and Benjamin, 1677; died
1689, aged 60, when wife and all children were living. References:
— ^Seoomb's Hist, of Aaiiherst, N. H., 580; Runnel's Hist, of
Sanibornton, N. H., II, 265; Essex Inst. Col., XXI, 79, 97; Paige's
Hist, of Hardwick, Mass., 368; Stiles' Hist, of Windsor, Conn., II, 208;
Young's Hist, of Chautauqua County, N. Y., 419, 643; Howel's Hist, of
Southampton, L. I., 2d ed., 241; Goodwin's Gen. Notes, 302;
Kellogg's White Gen., 31; Loomis Gen: Female Branches, 300;
Marshall's Granc Ancestry, 107; Strong Gen., 29!>; N. E. Hist, and
Gen. Reg., V, 458; Savage's Gen. Diet., II, 114. ELMENDORF
Sylvester's Hist, of Ulster County, N. Y., 102; Schoonmaker's Hist, of
Kingston, N. Y., 479; Munisell's N. Y. Coll., IV, 120; N. Y. Gen. and
BiO'g. Rec, XX, 101; Amer. Ancestry, vol. I, 26. Whittemore's Heroes
of the Revolution and their Descendants, 136. ELMER or ELLMER:—
Edward Elmer, of Cambridge, came in the"Lion,'' 1632, went early to
Hartford, oi w'hich he was one of the original proprietors, there had
Jolin, about 1645 ; Samuel, baptized 1647 ; Elizabeth, 1649; and
Edward, 1654; removed to Northampton, there haid Josepih, 1656;
Mary, 16.38; and he removed to Windsor, there 'had Sarah, about
1664. He was kiUed by the Indians in Philip's war, 1676. Of the wife
we know not the name nor the 'mother. References: — Temple's
Hist, of Northfield, JNIass., 437; Hyde's Hist, of BrimfieM, Mass.,
397; Stiles' Hist, of Wndsor, Conn., II, 234; Orcutt's Hist, of
Torrington, Conn., 687; Orcutt's Hist, of Stratford, Conn., 1197;
Sedgwick's Hist, of Sharon, Conn., 78; Littell's Passaic Valley, N. J,
148; Ellis Gen., 37:'.; Elmer Gen., 1840; Amer Ancestry, IX, 173,
223; Savage's Gen. Diet., II, 114. ELMORE. Powers' Hist, of
Sangamon County, III, 287; Amer. Ancestry, vol. I, 26; V, 28.
ELRICK'S. MaT.sihall Gen., 48. ELSE or ELSIE: — Elislia Els'c, oif
Newbury, freeman, 1673. Nicholas Else, New Haven, 1639, married
as second wife, Hanna'h, widow oif Robert Coe, oif Stratford, had
Samuel, 1666; di^d 1691. His widow died 1702. Roger Else,
Yarmouth, 1643, had John, baptized 1649; admitted an inhaibitanL
of Boston, 16.34, removed to Gharlestown, 1658, and died 1668.
ELSON, ELSEN or ELSING:— Abraham Elson_, Wethers'field, may
have been there 10 years, ibut died 1648, leaving two daughters His
widow married 1649, Jarvis Mudge. James Elson, of Gharlestown, by
wife Sarah, who died 1680, aged 38, had James, baptized 1672; and
Abigail, 1674. He was, tradition says, master of a ship taken by the
pirates of Algiers, 1678 or 9, and perhaps died in slavery. John
Elson, of Wethersfield, perhaps brother of Abraham, married a
widow who had sons Benjamin and Job and John; had no children of
his own, and died probably same time as Abraham. His widow
married Thomas Wright. John Elson, of Wells, freeman 1658, may
have been thie man at Cradock's plantation, 1631, called Elston;
foncdd by the Indian hostility, 1675, to Salem, where he died 1685,
leaving wtdow and six children. References: — lavage's Gen. Diet.,
[I, 115. ELTHAM:— William Eltham, of Woburn, had Hannah, 1690.
References:— Savage's Gen. Diet., II, 11,3. ELSTER. Buckingham
Gen., 112. ELSWORTH. Roome Cen., 104; Amer. Ancestry, V, 154.
ELTING. Sylvester's Hist, of Ulster County, N. Y., .34; Schoonmaker's
Hist, of Kingston, N. Y., 479; N. Y- Gen. and Bio'g. Rec, XVI, 25;
Anner. Ancestry, IV, 151. ELTON: — ^John Elton, of Middletown, by
wife Jane, had Mary, 1672; Richard, 1674; John, 1676; Richard,
again, 1679; Ann, 1681; and Efoenezer, 1686. A Mr. Elton, of
Sou'thoad, L. I., 1662, was admitted freeman of Conn, that year, and
may have been father of the preceding. References :—^Cregar's
White Gen.; Savage's Gen. Diet., II, 116. ELTONHEAD. Neil's Virginia
Carolorum, 251. ELWELL: — Robert Elwell, Of Dorchester, 1635,
removed 1638, to Salem, there had baptized, beside two others not
nameid, John, 1640 ; and Isaac, 1642 ; freeman 1640 ; removed to
Gloucester, was a sielectman 1648, and often after; had wife Jane,
Who died 1675, and he died 1683, but may have married 1676, Alice
Leach. He had Samuel; Josiah; Joseph; Sarah, 1651; Thomas,
baptized 1655; Jacob, born 16.57; Richard, baptized 1658; and
perhaps others. References :-^Farrow's Hist. of. Islesboroug-h, Me.,
203; Eaton's Hist, of Thomaston, Me., II, 211; Corliss' Hist, of North
Yarmouth, Me. ; Babson's Hist, of Gloucester, 87; Shaud's Hist, of
Fenwick Colony, N. J., 78; Savage's Gen. Diet., II, 116. ELWYN.
Wientworth Gen., vol. I, 337. ELY: — ^Nathaniel Ely, of Cambridge,
10;i2, freeman 16.35, removed, probably, next year to Hartford, was
an original proprietor, oonstable 1639, one of the first settlers at
Norwalk, 1651, and representative 1657, but removed to Springfield
three years laiter, and died there 1675. His widow Martha, died
1688. The only children we hear of are Samuel and Ruth; yet there
may have been other daughters. Richard Ely, of Sayhro'ok, had been
a merchant of Boston, 1664, and there married that year Elizabeth,
widow of John Cullick, and sister of Col. Fenwick. But' by a former
wife, he had, perhaps, not born on our side of the water, William and
RichaM; he died 1684; his wife died 1683. A Mr. Ely, a mariner, came
in the "Mayflower," 1620, but not as a passenger, to abide in the
land. He
 178 GENEALOGICAL GUIDE TO THE EARLY SETTLERS OF
AMERICA. was hired by the Pilgrims for a year, and ihad no -farther
relation to New England. Yet, as he was not one of the crew of the
vessel, but continued here till his time was out, the number is 102
besides the ship's company in that famous voyage. References: —
Long Meadow, Mass., Centen., 58; West Springfield, Mass., Centen.,
117; Orcutt's Hist, of Stratfor'd, Conn., 1197; Saunderson's Hist, of
CharlestOwn, N. H., 333; Darling Memorial; Goodrich's Recollections
of a Lifetime, vol. I, 533; Goodwin's Oloott Gen., 16; Hall's
Genealogical Notes, 106; Hill's Gen. Table of Lee Family, App. C. ;
Kellogg's White Gen., 65; Kitchell Gen., 52; Montague Gen., 83;
Walworth's Hyde Gen., II, 8;;8 ; Amer. Ancestry, HI, 78; VII, 137; N.
E. Hist, and Gen. Reg., XXXV, 23G; Savage's Gen. Diet., II, 116; Ely
Reunion; Ely Gen. BMBLIN: — John Bmblin, of Boston, minister of
the first Baptist Church from 1684, to his death, 1702. References:
— ^Savage's Gen. Diet., II, 116. EMBREE. Futhey's Hist, of Chester
County, Pa., 53. EMBRY. Meade's Old Farms of Va. EiM'ERICK. Amer.
Ancestry, II, 36. EMERSON: — John Emerson, of Ipswich, came in
the "Abigail," 1635, a baker, aged 20. It may be thai he removed to
Scituate, and married at Duxbury, lO^ii-^, Barbara, daughter of Rev.
John Lothrop. John Emerson, of Newbury, a lieutenant, bv wif':;
Judith, bad John, 1600; Daniel, 1()03; Joseph,' 1606: Samuel, 1600;
and Jonatihan, 1702. Michael Emerson, of Haverhill, 16.")6. Robert
Emerson, of Haverliill, freeman 16ii8, who had removed from
Rowley, where be was as early as Kio'o ; was killed by the Indians,
with his wife and children, Sarah and Timothy, 1607. Thomas
Emerson, o'f Ipswich, l(i:'>0, a baker, died 166'6; by wife Elizabeth,
bad Joseph, Nathaniel and James, Thomas and John. references.
Massachusetts. — Hammatt Papers Ipswich, 85: W)'man's
Charlestown Gens., vol. I, 331; Eaton's His't. of Reading, 68;
Babson's Hist .of Gloucester, 107: Maiden Bi-Centen., 244. Maine. —
^Dearborn's Hist, of Parsonfiield, :>7S; Poor's Llist. of Merrimac
Valley, 100, 171: Redlon's Harrison Settlers, 57; Eaton's Hist, of
Thomaston, II, 213. New Hampshire. — Worcester's Hist, o'f Hollis,
373; Runnel's Hist, of Sanbornton, II, 268; Secomb's Hist. Q.f
Amlierst, 5S1 ; Chase's Hist, of Chester, 516; Eaton's Hist, of Candia,
69: Fullerton's Plist. oif Raymond, 215; Coggswell's Hist, ol Henniker,
562; Hayward's His;, of Hancock, 55:5; Kidder's Hist, of New
Ipswich, 445; Morrison's Hist, of \A'incjham, 524; Livermore's Hist,
of Wilton, 363; New Hampshire Hist. Soc. Coll., ATI, 378 ;
Washington, N. H., Hist. 304; Wheeler's Hist, of Newport, 376;
Aldrich's Hist, of Walpole, 245. Other Publications. — Williams' Hist,
of Danby, Vt., 142; Walker Family, 24; Turner Gen.; Thompson's
Memoirs of Ebner Thompson ; Poore Gen., 75; Emerson Gen.;
Crane's Rawson Gen., S7 ; Cliapin Gen., 30!) ; Chapman's
Trowbridge Gen., 300 ; Blake's Hist, of Minidon Assn., 271; Amer.
Ancestry, V, S7; \^I, 185; XI, 20; Savage's Gen. Diet., II, 117.
EMERY or EMORY: — ^Anthony Emery, a carpenter, of Romsey, in
Hants, came in the "James," 1635, to Boston, perhaps with wife and
children, removed about 1644, to Dover, thence after 1648, to
Kittery ; was ferryman, kept an inn 1650, freeman 1652, constable
1658, representative 1680. Robert Emery, of New Haven. See
Ambry. George Emery, of Salem, a physician, had, says Felt, grant of
land 1637, was born 1609, land died 1687, his wife died 1673. James
Emery, of Kittery, perhaps brother of Anthony, freeman 1652,
constable 1670, and representative 1676, 7, 84, 5, and 92. John
Emery, of Newbury, 1635, brother of Anthony, came in the James,
1635, freeman 1641; brought son Jobn, bad here a daugbter
Ebenezer, 1648; and Jonathan, 1652. Noah Emery, of Kittery,
perhaps son of Anthony or John, escaped from the Indians 1693.
references: New Hampshire. — Dow's Hist, of Hampton, 702;
Cochrane's of Antrim, 485 ; Coggswell's Hist of Henniker, 564;
Cutter's Plist. of Jaffray, 309; Chase's Hist, of Chester, 518; Runnell's
Hist, of Sanbornton, II, 269. Maine. — Hatch's Hist, of Industry, 604;
Eaton's Hist, of Thomaston, II, 211; Maine Hist. Soc. Coll., IV, 2S!);
Poor's Hist, of Merrimac Valley, 119; Buxton Centen., 220; Farrow's
Hist, of Islesborough, 203. Other Publications. — Oofifin's Hist, of
Newbury, Mass., 301; Freeman's Hist, of Cape Cod, II, 6!)5 ;
/Vustin's R. I. Gen. Diet., 72; Benton's Hist, of Gui'.';lhall, \'t., 219;
Palmer Gen., 56; Guild's Stiles Gen., 32; Dudley Gen., 122; Amer.
Ancestry, 14, 37; VII, 121; IX, 212; N. E. Hist, and Gen. Reg. XXIII,
414; XXVII, 42:!; Savage's Gen. Diet., II, 118; Emery Gen. EMES.
Leonard's Hist, of Dublin, N. H,, 330. EM'LEN. Futhey's Hist, of
Chester County, Pa,, ."36. EMMERSON. Williams' Hiat. of Danby, 142.
EMMERTON. Drover Gen., :!43 ; Emmerton Gen. EMMES. Whitmore's
Copp's Hill Epitaphs. EMMET. Heraldic Journal, vol. 1, !)5, EMMETT.
Whitmore's Temple Gen. EMAIONS. Bergen's Hist. Kings County, N.
Y., 108. EMMONS: — tienry Emmons, of Boston, by wife Mary, had
Samuel, 1690. Thomas Emmons, of Newport, 163S, probably
removed to Boston, freeman 1652, died 1664, had daughter
Hannah, also Elizabeth, wife Martha, sons Ben amin, Obidiah and
Samuel. References: — Whittemore's Hist, of Middlesex County,
Conn., :'21; Bradbury's Hist, of Kennebunkport, 'Me., 242; North's
Hist, of Augusta, Me., 850; Temple's Hist, of North Brookfield, Mass.,
587; Babson's Hist, of Gloucester, Mass., 90; Blake's Hist, of Mindon
Association, 109; Spooner Gen., 210; Mack Gen., 16, 35; Blake Gen.,
4S; Savage's Gen. Diet., II, 119. EMORY. Stearns' Hist, of
Ashburnbam, Mass., 602; Stearns' Hist, of Rindge, N. H., 514.
EMPIE. Willis' Washington Gen., 281; Amer. Ancestry, II, 36. EMPY.
Pearson's Hist, of Schenectady, N. Y., 65.
 GENEALOGICAL GUIDE TO THE EARLY SETTLERS OF
AMERICA. 179 ENDICOTT:— Gilibert Endicott, of Reading, said to
have been born 1658, at D'orches'ter, but we know nothing more.
John Endicott, perhaps from Dorchester, England, by siome thought
his place of birth; born about 1589; came in the "Abigail," from
Weymouth, a small port in the channel, with wife and a small
company of about 20 or 30 others, including women and children, to
Salem, 1628. 'He was one of the six original purchasers of
Massachusetts B'ay from the Plymbuth Council, March preceding,
and the only one w'ho came over for more than two years. In the
Royal Charter of March following, he is named as an Assistant, one
of 18, and by his associates at London in General Court, after his
coming, made the bead superintendent, or governor, of the first
settlement at Salem, called London's plantation. He wias tihe
seventh Charter Governor of MassachuseUs, 1644. Honor enougih
there is for Endicott, the earliest patentee Who came over under the
indenture from the Plymiouth Company, without calling him "first
Governor of Massachusetts." He was the first and only Governor of
the London's Plantation, and if he ever was quialiiiied by taking the
oatlis under that delegation from the Governor and Company of
Massachusetts, which is unlikely and cannot be proven, he never had
a successor in that office, which was 'merged in the superior title on
arrival of Winthrop. As Assistant, he continued for '.I years, 'filo.m
1630, by successive elections ; except in 19:55, When for his
in'discreet zeal against the cross in the ensign, 'he was left out ; but
in 1636, 'he was made head of the first expedition against the
Pequots; for the first time, in 1641, deputy-governor according to
the Charter, and seven times a'fter, and in 1644, governor for the
first time, with full power according to the Charter, and again after
the death of Winthrop, 1649, 51, 2, 3, and fro'm 1655, to 'his death
at Boston, (w'here he had resided for about twenty years), 1666,
serving a longer period than any other of the Governors under the
old Charter, and by .Shirley alone exceeded, since, Endicott was of
stern energy, but great prudence in secular affairs, disapproving the
conduct of his friends in England, for putting to death their King, and
issued warrants for the apprehension of Whalley and Gofife, the
regicides, 'here. Much of the sad occurences of cruel scourging of
tbe Baptists 1651, and hanging of the Quakers 1659, that fell within
his administration, must be charged to Wilson and Norton, the
spiritual advisers of the day. His first wife was Ann Gower, who was a
cousin or niede of Matthew Cradock,, first Charter Governor, died
soon after cotninig, and she had, it is believed, no ciiildren; and he
married IKW. Elizabeth Gibson, fro'm Cambridge, England, had John,
1632 ; and Zerubbabel, about 1635. William Endicott, of Boston, a
mariner, in his will 1690, (he mentions son-in-law John Bell, and wife
Joanna. William Endicott, of Boston, by wife Elizabeth, had William,
1686; EHzabetn, 1600; John', 1693; Elizabeth, 1699; Benjamin,
1702; Lydia, 1703; LydLa, again, 1704; Sarah, 1705; Sarah, again,
1706; and Benjamin, again, 1709. References: — Perley's Hist, of
Boxford, Mass., 98; Moore's Mem. Am. Governors, vol. I, 363;
Dunstable Bi-Centennial, 176; Fehon Gen., 20; N. E. Hist, and Gen.
Reg., vol. I, 263, 335; Savage's Gen. Diet., H, 120. EN'DiILL:—
Michael Endill, Isle of Shoals, was grand juror at Court in York, 1659.
References: — ^Savage's Gen. Diet., II, 120. ENGLAND :^John
England, of New Haven, 1647, remioved to Branford, died 1655, left
widow, but no children. Pro'balbly another of this name in one of the
Providence Plantations, had daughter Ellen, who married 1665,
Jeremiah Westcott. References: — ^Powers' Hist, of Sangamon
County, III, 289; Futhey's Hist, of Chester County, Pa., 538; Cregar's
Haines Ancestry, 60; Austin's R. I. Gen. Diet., 72. EN'GLE:— Bernard
Engle, of Boston, 1664, husbandman. James Engle, of Boston, 1662,
mariner. References: — ^Cregar's Haines Gen., 18; Penn. Mag., IV,
353; Savage's Gen. Diet., II, 120. ENGLISH or ENGLES:— Clement
English, of Salem, married 1667, Mary, daughter of Ridbard Waters,
had Mary, 1669; Elizalbeth, 1671; Joseph, 1673; Benjamin, 1676j
Aibigaii, 1680; and Clement, 1683. The father died December
before, 1682. James English, of Boston, married 1658, perhaps as
second wife, Joanna, daughter of John Farnum, who was not 14
years old. We know too little of him to affirm or deny 'that he was
dead 1698, freeman 1691. Maudett English, of Boston, by wife Jane
had Hannah, 1639; Mary, 1644; his will names son Samuel, and
daughter-in4aw Mary; perhaps this daughter-in-law was the widow
English, who married 1688, Joshua Lee. Philip English, of Salem, son
of Jo'hn, of Isle of Jersey, there baptized 1651, a merchant, married
1675, Mary, daug'hter of Richard Hollingworth, suffered very mudh
in the blind ferocity against witchcraft. His wife was the greater
sufferer, and lived very few years after escape. This was managed
with skill and firmness by Rev. Joshua Moodey, then minister with
Willard in the Old South Church in Bioston. iHe had second wife
Saralh Ingersoll, was representative 170iO, one of the contributors
to the first Episcopal Church, 1734, and died 1740. He reckoned his
dajmage by the persecution at 1500 pounds sterling, and was
allowed about 20 years later 300 pounds sterling. Thomas English,
of Plymouth, one of the passengers of the "Mayflower," 1620, died
next spring, leaving no wife nor children. He was a sailor hired by
the Pilgrims. William English, of Ipswich, 1638, shoemaker, freeman
1642, representative 1646 and 7, .removed to Ham'pton, 1639, for
s'hort time, but went back to Ipswich. He may be the same who was
admitted at Boston, 1652, constable 1656, with wife Sarah, joined
our churc'h 1663. References: — ^Tuttle Family of Conn., 105;
Cunabell Gen., 36; Amer. Antestry, V, 81; VI, 28; VIII, 89. ENO,
EANNO, EiNNO or ENNOE:— James Eno, of Windsor, 1646, married
1648, Ann Bedwell, had Sarah, 1649; James, 1651; and John, 1654.
His wife died 1657, and he had second wife 1658, widow of
Tlhoimas Holcomb, who died 1679, and he married 1680, Esther,
widow of James Eggle&ton. He idled 1682. ENOW:— Thomas Enow,
Falmouth, 1689. References: — ^Stiles' Hist, of Windsior, Conn., II,
239; Orcutt's Hist, of Torrington, 687; Andrews' Hist, of New Britain,
Conn., 127; Barber's My Wife and M'other, App., 76; Bidwell Gen.,
Hayden's Virginia Gens., 24; Marshall's Grant Ancestry, 109; Savage's
Gen. Diet., II, 124; Howe's Barber and Eno Gen. ENOS. Power's Hist,
of Sangamon County, 111.,
 i8o GENEALOGICAL GUIDE TO THE EARLY SETTLERS OE
AMERICA. ENiSIGN: — James Ensign, of Cambridge, 1634, freeman
1035, removed about 1639 to Hartford, had only son David, and
three daughters, Sarah, Lydia, baptized 1649, and Alary; his will was
probated 1671. Thomas Ensign, of Sci^uate, married 1639,
Elizabeth Wilder, o'f Hingham, had Hannab, baptized 1640; Elizabeth
and John. He was of Duxbury, 1656, and died 1663. References: —
Winsor's Hist, of Duxbury, Mass., 257; Stiles' Hist, of Windsor, Conn.,
H, 248; Deane's Hist, 'of Scituate, Mass., 266; Amer. Ancestry, VII,
119; VIII, 214; Savage's Gen. Diet., II, 124. BDSOME:— Robert
Edsome, of Boston, 1646, merchant. References: — ^Savage's Gen.
Diet., II, 124. BNSOR. Mallorys Bobemia Manor. ENSWORTH,
ENDSWORTH or ENISWORTH: — Tixall, Tixoll, Texrhall or Tyxhall
Enswor.h, so variously written in records, was of Hartford, 1681,
removed 1700, to Canterbury, had baptized at Hartford, five
children, and left Nathaniel, Nebemiah, Ezra and Joseplh. ENYARD.
Clute's Hist, oi Staten Island, 380. ENYART. Powers' Hist, of
Sangamon County, 111., 380. EPES or EPPES: — Daniel Epes, of
Ipswich, son of Daniel, from Kent, England, oame 1637 with his
mother Martha, who is said to .have married Samuel Symonds. He
married 1644 Elizabeth, eldest daughter of Samuel Symonds, -wiho
died 1685, aged 60, by who'm he bad Samuel, 1G47; Daniel, 1649;
Nathaniel, 1650; John, 1651; Joseph, 1653; Martha, 1634; Mary,
1656; Lionel, 1657; another son, 1658; and Ricihard, 1659. He bad
second wife Lucy, daughter of Rev. John Woodbridge, widow of Rev.
Simon Bradstreet, of New London; was freeman 1674, a captain,
representative 1684, and died 169;;!, aged about 70 years.
References: — Hammatt Papers of Ipswich, 93; Slaughter's Bristol
Parish, Va., 172; Richmond, Va., Standard, II, 32; III, 16, 40;
Meade's Old Families of Va.; Page Gen., 105; N. E. Hist, and Gen.
Reg., XIII, 115; Savage's Gen. Diet., II, 125. ERB. Harris' Hist.
Lancaster County, Pa., 194. ERICHZON. Pearson's Hist, of
Schenectady, G~i. ERRINGTON. Paige's H:ist. of Camibridge, Mass.,
540. ERSKINE. Life of Rev. William Smith. ER\'ING. Prime's Bowdoin
Gen. ERTING. Cath. Hist. Coll., II, 333; Amer. Ancestry, III, 16; Yl,
30. ERRINGTON: — ^Abraham Errington, of Cambridge, 1649,
married Rebecca, daughter of Robert Cutler, of Charlestown, bad
Abraham, 1652; perhaps had a second Abrabam, 1654; Rebecca,
Hannah, Sarah, ]\Iary, baptized 1661; Abraham, 1663; and Jacob.
He died 1677, aged 55. Ann, probably his mother, died 1613, aged
76; but his father was, perhaps, dead before she caime over.
Thomas Errington, of Lynn, 1642, was of Charlestown, 1647, but
soon back to Lynn, and probably removed to ^^'arwick, there
freeman 1655. References: — Savage's Gen. Diet., II, 125. ERWIN:—
Edward Erwin, of Dover, 1658. References: — ^Savage's Gen. Diet.,
II, 125. ESMOND. Collins' Hist, o'f Hillsdale, N. Y., 53. ESSET: —
William Esset, of Boston, married Ann Sheffield, died 1697.
References: — ^Savage's Gen. Diet., II, 125. ESPY. Plumb's Hist, of
Hanover, Pa., 440; Kulp's Wyoming Valley Farms. Egle's Penn. Gens.,
177. BSSELSTYN. Munsell's Albany, N. Y., Coll., IV, 120 ; Amer.
Ancestry, II, 36. ESTABROOK or EASTERBROOK:— Josej^h
Estabrook, of Concord, came about 1660, from Enfievd, Middlesex,
England, it is said, with two brothers, graduated Harvard College,
1664, ordained about 1667, freeman 1665, married 1668, Mary,
daughter of Hugh Mason, had Joseph, 16(i.'); Benjamin, 1(171;
Mary, 10(3; Samuel, 1675; Daniel, 1677; and Ann, 1678. He died
1711. Thomas Estabrook, of Swanzey, by wife Sarah, had Elizabeth,
K;73. references. AIassachusetts. — Hudson's Hist, of Lexington, Gl;
Paige's Hist, of Cambridge, 541; Reed's Hist, of Rutland, 159 ;
Bond's Hist, of Watertown, 204 ; Cutter's Hist, of Arlington, 236;
Westminster, Mass., Centen., 32. Other Publications. — Washington,
N. H., Hist., ;".I4; Norton's Hist, of Fitzwilliam, N. H., 547; Hay\.'ard's
Hist, of Plancock, N. H., 563; Fowler's Chauncey Mem., 299;
Heminway's Vt. Gaz., V, 146; Amer. Ancestry, Yl, 62; Savage's Gen.
Diet., II, 126; Estabrook Gen. ESTERBROOK.- Amer. Ancestry, VII,
56. ESTAUGH. Clement's Hist, of Newtown, N. J. ESTEN : —
^Thomas Esten, of Providence, swore allegiance l(iS2. Referexies: —
^Austin's R. I. Gen. Diet., 294; Savage's Gen. Diet., II, 126. ILSTES:
— -Matthew Estes, of Dover, son of Robert, of D'over, England,
where be was born 1645, married 1(576, Philadelphia, daug'hter of
Reginald Jenkins, had Joseph, John, 1684; Richard, 1686; and
Matthew, 1689; possibly more. He probaby removed to Scituate, and
his wife died 1721; and he died 172:!. References: — ^Lapham's
Hist, of Woodstock, Me., 213; Lapham's Hist, of Bethel, Me., 525;
Bassett's Hist, of Richmond, N. H., 386 ; Barry's Hist, of Hanover
Mass., 307; Spooner Gen., vol. I, 484; Savage's Gen. Diet., H, 126;
Amer. Ancestry, III, 153, 205; IV, 42; Estes Gen. ESTEY. Heminway's
Vt. Gaz., V, 144; Amer. Ancestry, VIII, 100. ESTY. Thurston's Hist, of
Winthrop, Me., 181; Morrison's Hist, of Windham, N. H., 527; Morse
Mem. Appendix X, 20; Essex Inst. Coll., XVI, 104. BSTHERBROOKS.
Hodgman's Hist, of Westford, 445. ESTOW:— William Estow, of
Hampton, 1639, died 1 655 ; in his will names only daug'hters Sarah
and Mary. References: — Savage's Gen. Diet., II, 126. ETHEREDGE:
— Edward Etheredge, of Massachusetts, 1646. References: —
Savage's Gen. Diet., II, 126.
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 GENEALOGICAL GUIDE TO THE EARLY SETTLERS OF
AMERICA. ETHERINGTON :— Thomas'Etherington.of Kittery, was
lost, with 'his wife in the wreck of a small vessel, 1664. References:
— Savage's Gen. Diet., 11, 127. EUSTACE. Hayden's Virginia
Genealogies, 216. EUSTIS; — WilKam Eustis, o'f Charles'town, lived
at Maiden, perhaps Winisemet, or Boston, 1695, had, 1 suppose, son
William, perhaps other children, and w.fe Sara'h ,wiho died 1713,
aged 74. References: — ^Wyman's Charlestoiwn, Mass., Gens., vol.
I, 336; Reed's Hist, o'f Rutland, Mass., 127; N. E. Hist, and Gen.
Reg., XXXII, 204; Savage's Gen. Diet., II, 127. EVANCE:— Jo-hn
Evance, of New Haven, 1639, came probably, from London, signed
the origimal compact, was one of the most wealthy inhabitants, had
Daniel, baptized 1646; Mary and Stephen, 1652. He probably went
home, certainly was at London, 1656, and his widow Susanna,
married at London, Henry Hatsell. References: — Savage's Gen.
Diet., II, 127. EVAN. Smith's Delaware County, 459. EVANS: — 'David
Evans, of Bioston, 1654, merchant, died 1663, leaving widow Mary,
by whom he had Davi.l and Elizabeth, 1655; and Martha," 1657.
Henry Evans, of Boston, 1643, husbandman, freeman 1645; and his
wife Amy, came in the year preceding, from the church of Roxibury.
Administration on one Henry Evans, who was drowned 1667, was
granted in Middlesex, to his widow Esther. John Evans, of
Wethersfield, 1640, may have been at Hatfield, 1678. John Evans, of
Roxbury, by wife Mary, had John, baptized 1671; Peter, 1673; Peter,
again, 1674; it is tho'Ught he served in Philip's war. Perhaps he lost
his wife before or after he removed to Hatfield, there married 1677,
Mary, widow oi Experience Hinsdale, daughter of John Hawke, had
Elinor, 1678 ; Jonathan, 1680 ; and Randall, 1682; removed about
1685 to Deerfield. John Evans, of Dover, there acted as a
com'missioner with others to settle York, Dover and Kittery
boundary. Philip Evans, of Newbury, by wife Deborah, had William,
1687; Elizabeth, 1689; and John, 1692; the last at Ipswich. Richard
Evans, of Dorchester, freeman 1643, by wife Mary, had Richar
 I82 GENEALOGICAL GUIDE TO THE EARLY SETTLERS OF
AMERICA. John Evered, with a perpetual alias Webb, for surname, of
Boston, from Marlborough, in Wilts, came in the "James," lUoo, had
large estate from IGoO, as also at Chelmsford, where he was
Captain, and Representative, 1()63, i and 5, spent 'the last 5 or 6
years of his life in that part and died 1&68. His will names wife Mary,
and it may be presumed that he left no descendants. Stephen
Evered, perhaps brother of the preceding, having the same alias,
and coming in the same ship with him. William Evered, of
Charlestown, without the alias, married 1659, Sarah Fillebroiwn.
References: — iSavage's Gen. Diet., II, l:;:). EVEREST: — ^Isaac
Everest, o^f Guilford, by wife Joanna, had John, Isaac, 1(>(>7;
Benjamin and Lydla, died 1697, probably. Job Everest, brother c'f the
preceding, died 1684, unmarried. References: — Brown's West
Simsbury, Conn., Settlers, 59; Amer. Ances'try, II, 'M : Savage's Gen.
Diet., II, 130. EVERETT: — 'Francis Everett, of Reading, 107."),
married at Cambridge, Mary Edwards. Richard Everett, oif Dedham,
had, I presume, lived at Watertown, there proibably, by wife Mary,
had John, removed about 1636 or 7, 'had Mary, 1638; SamAiel,
1639; Sarah, Kill; and James, 1643; the mother died soon. He
married 1643, at Springfield, Mary Winch, had Sarah, again, 1644;
Abigail, ]li47; Israel, 1651; Ruth, 1(!."4 ; and Jedediah, 1656. He
died 168:3. Richard Everett, of Jamaica, L. I., had died in li.lM', or
earlier, for in that year Abraham Smith was appointed administrator
o'f his estate in trust for his children. These children are not named.
William Everett, whose name might be Averitt, of Kittery, 1640, was
admitted a freeman of Massachusetts, 165:2, when, perhaps, he
was of Dover, died at sea 1674. references. Massachusetts. — Hill's
Dedham Records; Temple's Flist. of. Northlield, 4:;9; Morse's Gen. of
Sherborn, Mass., 81; Jameson's Hist, of Medway, 4S2. Other
Publications. — Sedgwick's Hist, of Sharon, Conn., 79; Boyd's Annals
oif Winchester, Conn., 47; Baton's Hist, of Thomaston, Me., II, i!13;
Lapham's Hist, of Norway, Me., 498; Norton's Hist, of Fitzwilliam, N.
H., 548; Richmond, Va., Standard, IV, 5; Everett Gen.; Crawford
Family of Va., 79; Amer. Ancestry, IV, IS.-), 217; X. E. Hist, and Gen.
Reg., XIV, 215; Savage's Gen. Dio'., II, 130. EVERHART. Everhart
Gen. E\'ERIXGHAAI. Humphrey's Gen., 587, EVERILL: — ^Abiel
EveriU, oi Boston, married l(i55, Elizabeth, daughter of Lieut. Wilham
Phillips, had James, 165('); and died early, for his widow married
1660, John Alden, Jr. James Everill, of Boston, was admitted with
wife Elizabeth, of the church 1634, freeman 1635, had Ezekiel,
baptized l'>',) ; Deane's Hist, of Scituate, Mass., 267; Hayden's
Virginia Gens., 33:!; Savage's Gen. Diet., II, 132; Ewel'l Gen. EWER:
— ^Henry Ewer, of Sandwich, 1637. John Ewer, of Barnstable, died
1052. Thomas Ewer, of Charlestown, came in the "James," from
London, 10:15, aged 40; with wife Sarah, daughter of William
Earned, 28; and children Elizabeth, 4; and Thomas, 1-|; had elder
children, perhaps John, certainly Sarah; united with the church
1636, as had his wife the month before ; freeman 1636 ; died 1688 ;
and his widow married 1630, Thomas Lothrop, of Barnstable, where
his daughter Elizabeth was buried 1041. Thomas Ewer, of Sandwich,
of whom I learn nothing but that his widow Hannah, probated his
inventory 1067. Thomas Ewer, of Barnsta'ble, perhaps son of first
Thomas, had by first wife, Thomas, 1073, and probably m'other and
child died soon. He married second wife Elizabeth Lovell ,]0S4, who
died 1712, had Thomas, 1686; Shubael, 1690; John 1692;
Mehitable, 1694: Nathaniel, 1695; Jonathan, 1696; Hezekiah, 1697;
and Thankful, 1701; besides Sarah and Ehzabeth. References: —
'Swift's Barnstable, Mass., Families, vol. I, 360; Freeman's Hisit. of
Cape Cod, Mass., II, 151; Austin's Allied FamiHes of R. I., 92;
Savage's Gen. Diet., II, 132. EWILL:— John Ewill, of Newbury, 1669,
died 1686: Perha'DS it was soimetimes Ewins, and he may have
been son cf that William, who in 1666, was aged 46. References: —
^Savage's Gen. Diet., II, l:')2. EWIXG. Egle's Hist. Reg. Interior of
Penn., II, 206; Penn. Mag., VII, 94; Cooley's Trenton, N. J., 64;
Bwing Gen.
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