Chapter

A Review on Natural Antioxidants

Arun Rasheed and Rinshana Fathima Abdul Azeez

Abstract

Free radicals and related species have attracted a great deal of attention in recent
years. Oxidative stress has been considered a major contributory factor to the diseases.
They are mainly derived from oxygen (reactive oxygen species (ROS)) and nitrogen
(reactive nitrogen species (RNS)) and are generated in our body by various endog-
enous systems and exposure to different physicochemical conditions or pathophysi-
ological states. Free radical damage to protein can result in loss of enzyme activity.
There are epidemiological evidences correlating higher intake of components/foods
with antioxidant abilities to lower incidence of various human morbidities or mor-
talities. The sources and origin of antioxidants which include fruits and vegetables,
meats, poultry, and fish were treated in this study. The classification and character-
istics of antioxidant, its measurements and level in food and free radicals, were also
documented. The chemistry of antioxidants which includes chain reactions, molecu-
lar structures, food antioxidants and reaction mechanisms, biochemical activity,
therapeutic properties, and future choice of antioxidants was reported in this review.

Keywords: antioxidants, free radicals, oxidative stress

1. Introduction

Plants such as shrubs, herbs, or trees in parts or in whole were used in the treat-
ment and management of various diseases, and disorders can be dated long back.
Natural phytochemicals present at low levels in fruits, vegetables, herbs, and spices
offer many health benefits, but these compounds may not be effective or safe when
consumed at higher dose [1]. The presence of free radicals in biological materials
was discovered less than 50 years ago [2].
Pollutants, ionizing radiation or UV light, smoking, exposure of biological
systems to xenobiotics, and development of certain pathological conditions lead
to oxidative stress, thereby increases production of oxy radicals [3]. Cell damage
caused by free radicals appears to be a major contributor in aging and degenerative
diseases such as cancer, cardiovascular disease, cataracts, rheumatoid arthritis, and
brain dysfunction. Free radicals have been implicated in the pathogenesis of at least
50 diseases. Fortunately, free radical formation is controlled naturally by various
beneficial compounds and antioxidants, and its availability is limited that this dam-
age can become cumulative and debilitating. Antioxidants are capable of stabilizing,
deactivating, or scavenging free radicals before they attack cells.

Reactive species Symbol Half-life Reactivity/remarks

(in seconds)

Reactive oxygen species

Superoxide O2* 10−6 s Generated in mitochondria, in cardiovascular system, and others

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*
Hydroxyl radicle OH 10−9 s Very highly reactive, generated during iron overload and such
conditions in our body

Hydrogen H2O2 Stable Formed in our body by a large number of reactions and yields
peroxide potent species like. OH

Peroxyl radical ROO* S Reactive and formed from lipids, proteins, DNA, sugars, etc.
during oxidative damage

Organic hydroxide ROOH Stable Reactive with transient metal ions to yield reactive species
1
Singlet oxygen O2 10−6 s Highly reactive, formed during photosensitization and chemical
reactions

Ozone O3 S Present as an atmospheric pollutant can react with various

molecules

Reactive nitrogen species

Nitric oxide NO* S Neurotransmitter and blood pressure regulator can yield potent
oxidants during pathological status

Peroxy nitrile ONOO− 10−3 s Formed from nitric oxide and superoxide and highly reactive

Peroxynitrous acid ONOOH Fairly stable Protonated from of ONOO−

Nitrogen dioxide NO2 S Formed during atmospheric pollution

Antioxidants can be defined as substances whose presence in relatively low

concentrations significantly inhibits the role of oxidation of the targets. Due to
continuous generation of partially reduced forms of oxygen by constitutive meta-
bolic pathways, a number of protective antioxidant enzymes, such as superoxide
dismutase (SOD), catalase (CAT), glutathione peroxidase (GSHPx), glutathione
reductase (GSHRx), glutathione-S-transferase (GST), and nonenzymatic antioxi-
dants, have involved to deal with toxic species. Oxidation is a chemical reaction that
transfers electrons from a substance to an oxidizing agent. Oxidation reactions can
produce free radicals, which start chain reactions that damage cells. Antioxidants
terminate these chain reactions by removing free radical intermediates and inhibit
other oxidation reactions by being oxidized themselves. Antioxidants are often
reducing agents such as thiols, ascorbic acid, or polyphenols.

1.1 Sources and origin of antioxidants

Antioxidants are abundant in fruits and vegetables, as well as in other foods

including nuts, grains, and some meats, poultry, and fish. β-Carotene is found
in many foods, including sweet potatoes, carrots, cantaloupe, squash, apricots,
pumpkin, and mangoes. Lutein, best known for its association with healthy eyes,
is abundant in green, leafy vegetables such as collard greens, spinach, and kale.
Lycopene is a potent antioxidant found in tomatoes, watermelon, guava, papaya,
apricots, pink grapefruit, blood oranges, and other foods. Estimates suggest
85% of American dietary intake of lycopene comes from tomatoes and tomato
products [4].

1.1.1 Types of antioxidants

Antioxidants are grouped into two:

1. Primary or natural antioxidants

2. Secondary or synthetic antioxidants

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1.1.1.1 Primary or natural antioxidants

They are the chain breaking antioxidants which react with lipid radicals and
convert them into more stable products. They are mainly phenolic in structures and
include the following [5]:

1. Antioxidant minerals: These are cofactor of antioxidants enzymes. Their

absence will definitely affect metabolism of many macromolecules such as
carbohydrates. Examples include selenium, copper, iron, etc.

2. Antioxidant vitamins: They are needed for most body metabolic functions.
They include vitamin C, vitamin E, and vitamin B.

3. Phytochemicals: These are phenolic compounds that are neither vitamins nor
minerals. These include:

Flavonoids: These are phenolic compounds that give vegetables fruits, grains,
seeds leaves, flowers, and bark their colors. Catechins are the most active antioxi-
dants in green and black tea and sesamol. Carotenoids are fat soluble color in fruits
and vegetables. Zeaxanthin is high in spinach and other dark greens.

1.1.1.2 Secondary or synthetic antioxidants

These are phenolic compounds that perform the function of capturing free
radicals and stopping the chain reactions; the compound includes [5]:

1. Butylated hydroxyanisole (BHA)

2. Butylated hydroxytoluene (BHT)

3. Propyl gallate (PG) and metal chelating agent (EDTA)

4. Tertiary butylhydroquinone (TBHQ )

5. Nordihydroguaiaretic acid (NDGA).

2. Classification

• Enzymatic antioxidants:

1. Primary antioxidants, for example, SOD, catalase, glutathione peroxidase

2. Secondary enzymes, for example, glutathione reductase, glucose-6-phos-

phate dehydrogenase

• Nonenzymatic antioxidants:

1. Minerals, for example, zinc, selenium

2. Vitamins, for example, vitamin A, vitamin C, vitamin E

3. Carotenoids, for example, β-carotene, lycopene, lutein, zeaxanthin

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4. Low-molecular weight antioxidants, for example, glutathione, uric acid

5. Organosulfur compounds, for example, allium, allyl sulfide, indoles

6. Antioxidant cofactors

7. Polyphenols

2.1 Enzymatic antioxidants

2.1.1 Copper/zinc and manganese dependent

Superoxide dismutase (SOD): SOD is a group of endogenously produced

metalloenzymes with various prosthetic groups present both in prokaryotes and
eukaryotes [6]. Three main classes of them differ in their amino acid sequence
structure and metallic factors as follows:

1. Cu-Zinc SOD in the cytoplasm with two sub-units and sensitivity to cyanide
and hydrogen peroxide.

2. Mn SOD in the mitochondrial matrix and in prokaryotes and is insensitive to

cyanide.

3. Fe SOD, usually found in prokaryotes and in the chloroplasts of some plants. It

is not sensitive to cyanide but is inhibited by hydrogen peroxide.

4. Al SOD has recently reported [7].

Catalase: H2O2 is also metabolized by catalase (CAD), a heme protein with an

extremely high turnover rate

​
2 ​H​2​​O​2​→ 2 ​H​2​O + ​O​2​​

SOD protects from senescence, aging, ischemic tissue damage, lipid peroxida-
tion, protein denaturation, and radiation damage.
Glutathione peroxidase: Glutathione carries out the reduction of H2O2 which
is enzymatic reaction catalyzed by GPx, found in vacuole, cystol, and extracellular
space. The enzyme has substrate specificity. Peroxidases are involved in (1) biotic
and abiotic stresses, (2) lignin and suberin synthesis, and (3) disease and pathogen
response [8].

​
2 GSH + ​H​2​​O​2​→ GSSG + 2 ​H​2​O​

Consequence of H2O2 accumulation in glucose-6-phosphate dehydrogenase

deficiency due to malarial drug primaquine results in hemolytic anemia due to
oxidative stress.
Glutathione reductase: Glutathione keeps cysteine thiol groups in the reduced
state. If two thiol groups become oxidized, they can be reduced nonenzymati-
cally by glutathione. GSSG is reduced by NADPH-dependent enzyme glutathione
reductase.
+
​
GSSG + NADPH + H → 2GSH + ​NADP​​ ​​

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Glutathione-S-transferases: Through the action of this widely distributed

enzyme, glutathione participates in detoxification of xenobiotics or foreign organic
compounds.
Glutathione: Glutathione is a tripeptide that is present in high concentrations in
most eukaryotic cells and reacts with free radicals. It directly quenches lipid perox-
ides. Vitamin C and glutathione work interactively [9].

2.2 Nonenzymatic antioxidants

These are biological molecules that can act as antioxidants by either quenching
a free radical directly or indirectly by promoting a process responsible for radical
scavenging indirectly [10].

a. Selenium: Selenium is a mineral and a component of antioxidant enzymes.

Rice and wheat are the major dietary sources of selenium. The amount of sele-
nium in soil, which varies by region, determines the amount of selenium in the
foods grown in that soil. Animals that eat grains or plants grown in selenium-
rich soil have higher levels of selenium in their muscle. Brazil nuts also contain
large quantities of selenium.

b. Transferrin: Transferrin is a major iron transporting protein in the body. It is

normally 20–30% loaded.

c. Lactoferrin: Lactoferrin is a milk protein similar to transferrin that helps in

iron binding.

d. Ceruloplasmin: Ceruloplasmin catalyzes the oxidation of Fe++ to Fe+++, while

oxygen is reduced to water.

e. Vitamin A: Vitamin A is found in three main forms: retinol (vitamin A1),

3,4-didehydroretinol (vitamin A2), and 3-hydroxyretinol (vitamin A3). Foods
rich in vitamin A include liver, sweet potatoes, carrots, milk, egg yolks, and
mozzarella cheese.

f. Vitamin C (ascorbic acid): In the aqueous phase, ascorbic acid may reduce
reactive oxygen metabolites directly, with the concurrent formation of dehy-
droascorbate and/or indirectly by the regeneration of tocopherol from the
tocopherol radical [11]. Vitamin C can be found in high abundance in many
fruits and vegetables and is also found in cereals, beef, poultry, and fish.

g. Vitamin E: Vitamin E, also known as alpha-tocopherol, is found in almonds

and oils, including wheat germ, safflower, corn, and soybean oils, and is also
found in mangoes, nuts, broccoli, and other foods [12]. It reacts with reactive
oxygen metabolites, yielding lipid hydroperoxide, which can be removed by
the activity of the phospholipase-GSPHx system.

h. β-Carotene: β-Carotene is a lipid-soluble precursor of vitamin A. It functions

synergistically with tocopherol to prevent lipid peroxidation.

i. Ubiquinol-10: It is a reduced form of coenzyme Q10, present in lipoprotein

at relatively low concentrations. It probably regenerates tocopherol from the
tocopheroxyl radical and increases its antioxidant efficiency.

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2.3 Plant-derived antioxidants

To protect the cells and organ systems of the body against ROS, humans have
evolved a highly sophisticated and complex antioxidant protection system. It
involves a variety of components, both endogenous in origin, that function interac-
tively and synergistically to neutralize free radicals [13].
These components include:
Nutrient-derived antioxidants like ascorbic acid, tocopherols and carotenoids,
and other low-molecular weight compounds such as GSH and lipoic acid.
Antioxidant enzymes, for example, SOD, GSHPx and GSH reductase, which
catalyze free radical quenching reactions.
Metal-binding proteins such as ferritin, lactoferrin, albumin, and ceruloplasmin
that sequester free iron and copper ions as these ions are capable of catalyzing
oxidative reactions.
Numerous other antioxidant phytonutrients present in a wide variety of plant
foods.

3. Antioxidant operation and mechanisms

The word antioxidant is used in a general sense to refer to any type of chemical
agent which inhibits attack by oxygen or ozone [14]. As applied to vegetable oils,
antioxidants are compounds which interrupt the oxidation process by preferentially
reacting with the fat radical to form a stable radical which does not quickly react
with oxygen [15]. Antioxidants function either by inhibiting the formation of
free alkyl radicals in the initiation step or by interrupting the propagation of the
free radical chain. In truncating the propagation step, the antioxidants function
as hydrogen donors. Generally, the most popular antioxidants are hydroxyphenol
compounds with various ring substitutions. The antioxidant radical is stabilized
with its local electrons delocalized; hence antioxidant free radicals do not readily
initiate other free radicals. They rather even react with lipid free radicals to form
stable and complex compounds. In investigating phenolic antioxidants, it is found
that their antioxidative capabilities bear a relationship to the number of phenol
groups occupying 1,2 or 1,4 positions in an aromatic ring as well as to the volume
and electronic characteristics of the ring substituents present [16]. In elucidating
the mechanism of oxidative inhibition, it is generally established that antioxidants
function as oxygen interceptors in the oxidative process thereby breaking the chain
reaction that perpetuates the process [17]. The general scheme is presented below:

​
R + AH → RH + A​

​
RO + AH → ROH + A​

​
ROO + AH → ROOH + A​

​
R + A → RA​

​
RO + A → ROA​

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​
ROO + A → ROOA​

​
Antioxidant + ​O​2​→ Oxidized antioxidant​

Certain metallic ions such as copper and iron act as prooxidants, catalyzing the
oxidation process. Such metal ions can be sequestered or chelated by certain organic
acids. They effectively contribute to lower transition metal activity. Examples of
such compounds are citric acid, phosphoric acid, and some of their derivatives.

4. Estimation of antioxidants

4.1 Conjugated diene assay

This method allows dynamic quantification of conjugated dienes as a result of

initial PUFA (polyunsaturated fatty acids) oxidation by measuring UV absorbance
at 234 nm. The principle of this assay is that during linoleic acid oxidation, the
double bonds are converted into conjugated double bonds, which are characterized
by a strong UV absorption at 234 nm. The activity is expressed in terms of inhibi-
tory concentration (IC50) [17, 18, 19].

4.2 DPPH method (1,1 diphenyl-2-picrylhydrazyl)

This most widely reported DPPH assay method is based on the reduction of
methanolic solution of colored free radical DPPH by free radical scavenger. The
procedure involves measurement of decrease in absorbance of DPPH at its absorp-
tion maxima of 516 nm, which is proportional to concentration of free radical
scavenger added to DPPH reagent solution. The activity is expressed as effective
concentration EC50 [20].

4.3 Superoxide radical scavenging activity

In vitro superoxide radical scavenging activity is measured by riboflavin/light/

NBT (Nitro blue tetrazolium) reduction. NBT method is based on generation of
superoxide radical by auto-oxidation of riboflavin in presence of light. The super-
oxide radical reduces NBT to a blue-colored formazan that can be measured at
560 nm. The capacity of extracts to inhibit the color to 50% is measured in terms of
EC50. Antioxidant activity of Ailanthus, flavonoids, and triphala has been reported
in terms of superoxide radical scavenging activity. The superoxide radical can also
be detected by oxidation of hydroxylamine, yielding nitrite which is measured
colorimetric reaction [21, 22].

4.4 Hydroxyl radical scavenging activity

This method involves in the in vitro generation of hydroxyl radicals using

Fe3+/ascorbate/EDTA/H2O2 system using Fenton reaction. Scavenging of this
hydroxyl radical in presence of antioxidant is measured. In one of the methods, the
hydroxyl radicals formed by the oxidation is made to react with DMSO (dimethyl
sulphoxide) to yield formaldehyde. Formaldehyde formed produces the intense
yellow color with Nash reagent (2 M ammonium acetate with 0.05 M acetic acid and
0.02 M acetyl acetone in distilled water). The intensity of yellow color formed by

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that reaction is measured at 412 nm spectrophotometrically against reagent blank.

The activity is expressed as % hydroxyl radical scavengering [21].

4.5 Nitric oxide radical inhibition activity

Nitric oxide, because of its unpaired electron, is classified as a free radical and
displays important reactivities with certain types of proteins and other free radicals.
In vitro inhibition of nitric oxide radical is also a measure of antioxidant activ-
ity. This method is based on the inhibition of nitric oxide radical generated from
sodium nitroprusside in buffer saline and measured by Griess reagent. In presence
of scavengers, the absorbance of the chromophore is evaluated at 546 nm. The
activity is expressed as % reduction of nitric oxide [21].

4.6 Reducing power method

This method is based on the principle of increase in the absorbance of the

reaction mixture, which indicates increase in the antioxidant activity. In this
method, antioxidant compound forms a colored complex with potassium fer-
ricyanide, trichloroacetic acid, and ferric chloride, which is measured at 700 nm.
Increase in absorbance of the reaction mixture indicates the reducing power of
the samples [23].

4.7 Phosphomolybdenum method

A spectroscopic method for the quantitative determination of antioxidant

capacity, through the formation of phosphomolybdenum complex. The assay is
based on the reduction of Mo (VI) to Mo (V) by the sample and subsequent forma-
tion of a green phosphate Mo (V) complex at acidic pH [24].

4.8 Peroxynitrite radical scavenging activity

Peroxynitrite is now recognized by researchers as the culprit in many toxic

reactions. Hence, an in vitro method for scavenging of peroxy radical has been
developed to measure antioxidant activity. The scavenging activity is measured
by monitoring the oxidation of dihydrorhodamine on a microplate fluorescence
spectrophotometer at 485 nm [25].

4.9 ABTS (2,2-azino-bis(3-ethyl benzothiazoline-6-sulfonic acid) diammonium

salt) method

This is a measure of antioxidant activity. It also permits to distinguish between

additive and synergistic effects. The assay is based on interaction between antioxi-
dant and ABTS+ radical cation which has a characteristic color showing maxima at
645, 734 and 815 nm [24–26].

4.10 DMPD (N,N-dimethyl-p-phenylenediamine dihydrochloride) method

This assay is based on the reduction of buffered solution of colored DMPD in

acetate buffer and ferric chloride. The procedure involves measurement of decrease
in absorbance of DMPD in presence of scavengers at its absorption maxima of
505 nm. The activity was expressed as percentage reduction of DMPD [24–27].

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4.11 Oxygen radical absorbance capacity (ORAC)

ORAC is an exciting and revolutionary new test tube analysis that can be utilized
to test “antioxidant power” of foods and other chemical substances. It calculates the
ability of a product or chemical to protect against potentially damaging free radicals.
This analytical procedure measures the ability of a substance to act as an antioxidant.
The test is performed using Trolox (a water-soluble analog of vitamin E) as a stan-
dard to determine the Trolox equivalent (TE). The ORAC value is then calculated
from the Trolox equivalent and expressed as ORAC units or value. From this assay it
shows the higher the ORAC value, the greater the “antioxidant power.” In automated
ORAC assay B-phycoerythrin (b-PE) was used as a target free radical damage, AAPH
as a peroxy radical generator and Trolox as a standard control. After addition of
AAPH to the test solution, the fluorescence is recorded, and the antioxidant activity
is expressed as Trolox equivalent [28].

4.12 β-Carotene linoleate model

This is one of the rapid methods to screen antioxidants, which is mainly based
on the principle that linoleic acid, which is an unsaturated fatty acid, gets oxidized
by “reactive oxygen species” (ROS) produced by oxygenated water. The products
formed will initiate the β-carotene oxidation, which will lead to discoloration.
Antioxidants decrease the extent of discoloration, which is measured at 434 nm,
and the activity is measured [24].

4.13 TRAP method

This method is defined as total radical trapping antioxidant parameter. The fluo-
rescence of R-phycoerythrin is quenched by ABAP (2,2′-azobis(2-amidinopropane)
hydrochloride) as a radical generator. The antioxidative potential is evaluated by
measuring the delay in decoloration [29].

4.14 Cytochrome c test

Superoxide anions were assayed spectrophotometrically by a cytochrome

reduction method described by McCord [6]. Xanthine oxidase converts xanthine to
uric acid and yields superoxide anions which directly reduce ferricytochrome c to
ferrocytochrome c, having an absorbance change at 550 nm. [30].

4.15 Erythrocyte ghost system

This method involves isolation of erythrocyte ghost cells and the induction of
lipid peroxidation using them and the induction of tetra-butyl hydroxy peroxide
(t-BHP). Thiobarbituric acid reactive substance (TBARS) produced during the
reaction is measured at 535 nm [31].

4.16 Microsomal lipid peroxidation or thiobarbituric acid (TBA) assay

TBA test involves isolation of microsomes from rat liver and induction of lipid
peroxides with ferric ions leading to the production of small amount of malondi-
aldehyde (MDA). TBA reacts with MDA to form a pink chromogen, which can be
detected spectrophotometrically at 532 nm [32].

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5. The potential role of antioxidants in disease

5.1 Oxidative stress and diseases

5.1.1 Nephrotic syndrome

The nephrotic syndrome (NS) is defined by heavy proteinuria (urine total protein
excretion greater than 3.5 g/d or total protein-creatinine ratio greater than 3.5 g/g) due
to abnormal increase of glomerular permeability and following hypoalbuminemia,
hyperlipidemia, and edema. Peroxidation of lipid membranes raises the concentration
of their by-product MDA and the consequent lowering of antioxidants as a result of
consumption [33]. The combined therapy of antioxidants, minerals with B complex
vitamins for treatment of imbalance oxidant/antioxidant status, hyperhomocyst(e)
inemia, and deficiency of copper and zinc in nephrotic syndrome patients.

5.1.2 Oxidative stress and neurodegenerative diseases

The brain is exposed throughout life to OS, and certain diseases of the brain and
nervous system are thought to involve free radical processes and oxidative damage,
either as a primary cause or as a consequence of disease progression.

1. Alzheimer’s disease: Alzheimer’s disease (AD) is a progressive neuropsychiat-

ric disorder of unknown etiology. It is characterized by neuronal degeneration
and cognitive deterioration, especially in the elderly [34]. OS has been impli-
cated in the pathogenesis of AD [35] by the finding of several characteristics,
such as enhanced lipid peroxidation, in specific areas of the brain in post-
mortem studies [36]. Several investigators detected an increase in the activity
of catalase, superoxide dismutase, glutathione peroxidase, and glutathione
reductase in the hippocampus and amygdale.

2. Cognitive dysfunction in the elderly: Cognitive impairment is a common

problem in the over 65-year age group, progressing to its most devastating
form of clinical dementia, usually Alzheimer’s dementia, in about 5% of this
population [37]. Goodwin noted a correlation between memory function and
vitamin C in the blood of healthy volunteers aged 60 or over [38]. Accordingly,
Perry found a positive association of memory performance with β-carotene
and vitamin C levels in plasma measured twice [39].

3. Parkinson’s disease: Data from postmortem studies of brains from patients

with Parkinson’s disease (PD) suggest that OS plays an important role in neural
degeneration of the pigmented dopaminergic neurons in the substantia nigra
pars compacta (SNpc) [40]. One of the suggested causes of OS in the SNpc
is the production of ROS during the normal metabolism of dopamine. In the
human SNpc, the oxidation products of dopamine may polymerize to form
neuromelanin, which may also be toxic [41, 42]. According to postmortem
studies, the SNpc of PD patients shows a significant (60%) reduction in GSH
and a moderate (29%) increase in oxidized glutathione (GSSG) levels [43, 44].

4. Huntington’s disease: Huntington’s disease is an autosomal neuronal disorder

characterized as a movement disorder caused by repetition of a CAG trinucleo-
tide sequences encoding for a polyglutamine tract at the N terminus of the gene
encoding a protein named huntingtin [45]. Several postmortem studies showed
increased iron levels in the striatum of patients with Huntington’s disease [46].

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5. Amyotrophic lateral sclerosis (ALS): ALS is characterized by a selective and

progressive degeneration of the lower motor neurons in the spinal cord and the
upper motor neurons in the cerebral cortex, usually beginning in midlife. OS
may be involved in all types of ALS [47]. Levels of vitamin E and malondial-
dehyde (MDA), as a measure of lipid oxidation, increased over time in mutant
CuZnSOD mice, as compared to controls [48].

6. Schizophrenia and tardive dyskinesia: The presence of excess levels of ROS

has been described for both schizophrenia and neuroleptic-induced tardive
dyskinesia [49]. The contribution of oxidative injury to the pathophysiology of
schizophrenia is indicated by the increase in lipid peroxidation products in the
plasma and CSF and the altered levels of both enzymatic and nonenzymatic
antioxidants in chronic naive first-episode patients [50, 51].

7. Chemically induced neurological disorders: Several neurotoxic chemicals

have been shown to elevate the cerebral rate of ROS production in experimen-
tal animals. These include methylmercuric chloride, cadmium, toluene, and
other organic solvents [52, 53]. All of these agents are also capable of increas-
ing intracellular levels of calcium ions [54].

8. Brain aging: Aging in mammalian species appears to be the result of normal

developmental and metabolic processes responsible for graying of the hair,
decreases in the rate of wound healing, and increases in susceptibility to disease
and death. Studies have found evidence of oxidative damage to macromolecules
(DNA, lipids, and proteins) especially in brains from elderly subjects, support-
ing the hypothesis that oxidative injury might directly cause the aging process
[55–57].

5.1.3 Diabetes mellitus

Diabetes in humans is a disease associated with increased oxidative stress.

The cause of this is not yet fully understood but is thought to include mitochon-
drial dysfunction, direct enzyme inhibition by hyperglycemia, auto-oxidation of
glucose, and activation of NADPH oxidase. The oxidative stress manifests itself
as elevated concentrations of lipid peroxidation products, erythrocyte fragility,
and decreases in the antioxidant enzyme systems (CAT, GSH-PX, and SOD)
[58–61].

5.1.4 Asthma

Feline asthma closely parallels human asthma, which is known to be associated

with oxidative stress. Such cells generate ROS, which are involved in the patho-
physiology of asthma [62, 63].

5.1.5 Atherosclerosis

It has been known that LDL can be oxidized by many kinds of oxidants by dif-
ferent mechanisms and pathways. Myeloperoxidase (MPO) secreted from phago-
cytes has been implicated in the pathogenesis of atherosclerosis. Reactive nitrogen
species are another species, which may contribute in atherosclerosis. Nitric oxide
(NO) is not a strong oxidant in itself, but it reacts rapidly with O2 to give peroxyni-
trite, which oxidizes LDL to an atherogenic form [64].

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5.1.6 Heart failure

Accumulating evidence suggests that reactive oxygen species (ROS) play an

important role in the development and progression of heart failure, regardless of
the etiology.

5.1.7 Hemorrhagic shock

Acute hemorrhagic shock causes decreases in the cardiac function and contrac-
tility and is associated with an increase in oxygen free radical (OFR) producing
activity of PMN leukocytes [65].

5.1.8 Ischemia–reperfusion

Reactive oxygen-derived radicals and metabolites are known to play important

roles in the pathogenesis of ischemia/reperfusion and anoxia/reoxygenation injury.
Free radicals are induced by the reperfusion blood flow in addition the lack of
oxygen (O2) supply to the ischemic cell.

5.1.9 Lung disease

The large endothelial surface is constantly exposed to many atmospheric pol-

lutants including tobacco smoke, fuel emissions, ozone, and nitrogen dioxide, and
given the natural oxidizing nature of the atmosphere (e.g., 21% O2), the lung is
always at risk of oxidative injury [66].

5.1.10 Aging

The free radical theory of aging includes phenomenological measurements of

age-associated oxidative stress, interspecies comparisons, dietary restriction, the
manipulation of metabolic activity and oxygen tension, treatment with dietary and
pharmacological antioxidants, in vitro senescence, classical and population genet-
ics, molecular genetics, transgenic organisms, the study of human diseases of aging,
epidemiological studies, and the ongoing elucidation of the role of active oxygen in
biology [67].

5.1.11 Free radicals and cancer

One type of endogenous damage is that arising from intermediates of oxygen

(dioxygen)-reduction oxygen free radicals, which attacks not only the bases but also
the deoxyribosyl backbone of DNA. OFR are also known to attack other cellular
components such as lipids, leaving behind reactive species that in turn can couple to
DNA bases [68].

5.1.12 Inflammation

During phagocytosis, cells consume increased amount of oxygen, a process

termed the respiratory burst. Activation results in increased NADPH production via
the hexose monophosphate shunt, and the generation of O2, H2O2, OH and hypo-
chlorous acid (HOCI), hypoxanthine concentration, xanthine oxidase activity, and
ROS production are increased in rheumatoid arthritis [69].

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5.1.13 Ocular disease

Oxidative stress is implicated in age-related macular degeneration and cataracts

by altering various cell types in the eye either photochemically or nonphotochemi-
cally [70]. Under the action of free radicals, the crystalline proteins in the lens can
cross-link and aggregate, leading to the formation of cataract [71, 72].

5.1.14 Fetus

Oxidative stress is involved in many mechanisms in the development of fetal

growth restriction and preeclampsia in prenatal medicine. Some reports indicate
that blood levels of lipid peroxidation products (F2-isoprostanes, MDA) are
elevated in preeclamptic pregnancy and intra-uterine growth retardation, and
it has been suggested that ROS/RNS play a role in the etiology of these diseases
[63, 73]. In pregnancies complicated by preeclampsia, increased expression
of NADPH oxidase 1 and 5 isoforms which are the major enzymatic sources of
superoxide in the placenta is seen [74].

S. no Plant name Family Part Chemical constituents responsible for Reference(s)

used antioxidant activity

1 Amaranthus Amaranthaceae Leaf Carotenoids, ascorbic acid, flavonoids, and [75]

paniculatus phenolic acids

2 Amaranthus Amaranthaceae Leaf Carotenoids, ascorbic acid, flavonoids, and [75]

gangeticus phenolic acids

3 Amaranthus Amaranthaceae Leaf Carotenoids, ascorbic acid, flavonoids, and [75]

blitum phenolic acids

4 Amaranthus Amaranthaceae Leaf Carotenoids, ascorbic acid, flavonoids, and [75]

spinosus phenolic acids

5 Amaranthus Amaranthaceae Leaf Carotenoids, ascorbic acid, flavonoids, and [75]

viridis phenolic acids

6 Coriandrum Umbelliferae Leaf, S-(+)-linalool, monoterpenes, [76]

sativum fruit hydrocarbons, namely, α-pinene,
limonene, γ-terpinene, p-cymene, borneol,
citronellol, camphor, geraniol, and geraniol
acetate, heterocyclic components like
pyrazine, pyridine, thiazole, furan and
tetrahydrofuran derivatives, isocoumarins,
coriandrin, dihydrocoriandrin, coriandrons
A–E, flavonoids, pthalides, neochidilide,
digustilide phenolic acids, and sterols

7 Emblica Umbelliferae Fruit, Vitamins, ascorbic acid, and phenolics [76]

officinalis leaves are known as hydrophilic antioxidants,
while carotenoids are known as lipophilic
antioxidants

8 Digera Amaranthaceae Leaf Phenols, flavonoids, glycosides, tannins and [76]

muricata (L.) terpenoids, and minimum for saponins

9 Chenopodium Amaranthaceae Leaf Alkaloids, apocarotenoids, flavonoids, [77]

album L. phytoecdysteroids xyloside, limonene
(23.2%), α-terpinyl acetate (13.7%),
α-terpinene (12.3%), and cis-ascaridole
(12.2%)

13
Traditional and Complementary Medicine

S. no Plant name Family Part Chemical constituents responsible for Reference(s)

used antioxidant activity

10 Basella alba Basellaceae Leaf Proteins, fat, vitamin A, vitamin C, vitamin [78]
Linn E, vitamin K, vitamin B9 (folic acid),
riboflavin, niacin, thiamine, and minerals
such as calcium, magnesium, iron

11 Basella rubra Basellaceae Leaf Calcium, iron, vitamins A, B, and C, [79–81]

saponins A, B, C, and D, oleanane-type
triterpene oligoglycosides, spinacoside C,
and momordins IIb and IIc, β-carotene,
small amounts of α-carotenes, 4-coumaroyl,
and feruloyl derivatives

12 Physalis Solanaeae Leaf, 2,3-Dihydro-3beta-methoxyixocarpalactone [82]

philadelphica fruit A, 2,3-dihydro-3beta-
methoxyixocarpalactone B,
2,3-dihydroixocarpalactone B

13 Rumex Polygonaceae Leaf Minerals, protein and ascorbic acid, oxalic [83]
vesicarius acid, tocopherol and lipids. Ca, Cu, Fe, Mg,
K, Na, Zn, lipids, ascorbic acid, tocopherol

14 Paederia foetida Rubiaceae Leaves Β-Sitosterol, leupiol, methyl mercaptan, [84]

crystalline keto alcohol, paederolone,
paederone, and hetasitosterol

15 Solanum Solanaceae Leaf Acetic acid, tartaric acid, malic acid and [85]
nigrum Linn citric acid, solanine, alpha, beta gamma
chaconines, and alpha, beta gamma
solanines, solanine, beta-2-solamargine,
solamargine, and degalactotigonin. Five
non-saponins including p-hydroxybenzoic
acid and 3-methoxy-4-hydroxybenzoic acid

16 Trigonella Leguminosae Leaf Amino acid, fatty acid, vitamins, [86]

foenum- saponins, folic acid, disogenin, gitogenin,
gracecum Linn neogitogenin, homorientinsaponaretin,
neogigogenin, and trigogenin, 4,5[delta]-
cadinene (27.6%), [á]-cadinol, palmitic
acid, linoleic acid, oleic acid and stearic
acid, hexanal, 2-methyl-2-butenal,
3-octen-2-one, flavonoids, polysaccharides,
saponins, polysaccharides, trigonelline,
choline, quercetin, galactomannan,
polysaccharides

17 Brassica Brassicaceae Leaf Glucosinolates and their derived products, [87]

oleracea flavonoids, and other phenolics, quercetin
Capitata 3-O-sophoroside-7-O-glucoside,
3-p-coumaroylquinic acid, kaempferol-3-
O-sophoroside-7-O-glucoside, kaempferol
3-O-(caffeoyl)-sophoroside-7-O-glucoside,
sinapoyl glucoside acid, kaempferol
3-O-(sinapoyl)-sophoroside-7-O-
glucoside, sinapic acid, 3 isomeric forms
of 1,2-disinapoylgentiobiose, kaempferol
3-O-sophoroside-7-O-glucoside

18 Moringa Moringaceae Leaf 4-(4’-O-Acetyl-α-L-rhamnopyranosyloxy) [88]

pterygosperma benzyl isothiocyanate, 4-(α-L-
Gaertn rhamnopyranosyloxy)benzyl
isothiocyanate, niazimicin,
pterygospermin, benzyl isothiocyanate,
and 4-(α-L-rhamnopyranosyloxy)benzyl
glucosinolate, carotenoids (including
β-carotene or pro-vitamin A)

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A Review on Natural Antioxidants
DOI: http://dx.doi.org/10.5772/intechopen.82636

S. no Plant name Family Part Chemical constituents responsible for Reference(s)

used antioxidant activity

19 Hibiscus Malvaceae Leaf Tannins, saponins, polyphenolics, alkaloids, [89]

cannabinus L lignans, essential oils, and steroids

20 Sesbania Fabaceae Leaf Galactomannans, linoleic acid, β-sitosterol, [90–92]

grandiflora L and carbohydrates. Vitamin C, and
calcium, iodine, pectin, saponins, aliphatic
alcohol, leucocyanidin and cyanidin,
oleanolic acid and its methyl ester and
kaempferol-3-rutinoside, tannins and
gum, sesbanimide

21 Portulaca Portulacaceae Leaf Omega-3 fatty acids, gallotannins, [93–95]

oleracea L kaempferol, quercetin, apigenin,
α-tocopherols, ascorbic acid and
glutathione, free oxalic acids, β-carotene,
omega-3 fatty acids, coumarins, flavonoids,
monoterpene glycoside, and anthraquinone
glycosides

22 Murraya Rutaceae Leaf Alkaloid, volatile oil, glycozoline, [96–100]

koenigii L xanthotoxin, and sesquiterpine

23 Celosia argentea Amaranthaceae Leaf Alkaloids, glycosides, flavonoids, saponins, [101]

tannins, carbohydrate and essential oils,
steroids, carotenoids, and anthocyanins

24 Boerhavia Nyctaginaceae Leaf Alkaloids, punarnavine, rotenoids [102–109]

diffusa (boeravinones A–F), amino acids,
lignans (liriodendrons), ß-sitosterols
and tetracosanoic, esacosanoic, stearic,
and ursolic acids. Rotenoids known as
boeravinones, punarnavoside, a phenolic
glycoside, 11,12 C-methyl flavone
liriodendrin and syringaresinolmono-
β-D-glycoside, fatty acids and allantoin
boerhavin and boerhavic acid, aegeline,
aegelinine, rutin, sterol, tannins,
flavonoids, quercetin, volatile oils,
ß-sitosterols

25 Eclipta alba Asteraceae Leaf Coumestans, alkaloids, flavonoids, [110]

glycosides, polyacetylenes, triterpenoids,
and thiophenes. Phytosterol, P-amyrin,
luteolin-7-glucoside, P-glucoside of
phytosterol, a glucoside of a triterpenic
acid and wedelolactone. Cystine, glutamic
acid, phenylalanine, tyrosine and
methionine, nicotine, and nicotinic acid

26 Centella Apiaceae Leaf Asiaticoside carotene, ascorbic acid, [111]

asiatica phenols, madecassic acid

27 Phyllanthus Euphorbiaceae Leaf Alkaloids, astragalin, brevifolin, [112]

amarus carboxylic acids, corilagin, cymene,
ellagic acid, ellagitannins, gallocatechins,
geraniin, hypophyllanthin, phyllanthin,
lignans, lintetralins, lupeols, methyl
salicylate, phyllanthine, phyllanthenol,
phyllochrysine, phyltetralin, repandusinic
acids, quercetin, quercetol, quercitrin,
rutin, saponins, triacontanal, and
tricontanol
28 Hibiscus Malvaceae Leaf Ascorbic acid (vitamin C) and tocopherol [83]
sabdariffa (vitamin E), flavonoids, polyphenols

15
Traditional and Complementary Medicine

S. no Plant name Family Part Chemical constituents responsible for Reference(s)

used antioxidant activity

29 Curcuma longa Zingiberaceae Leaf Ascorbic-acid rhizome,beta-carotene [113]

rhizome, caffeic-acid rhizome, curcumin
rhizome, eugenol essential oil, p-coumaric-
acid rhizome, protocatechuic acid leaf,
syringic-acid leaf, vanillic acid in leaf,
camphene, eugenol, curcumin

30 Ocimum Labiatae Leaf Volatile oil, terpenoids, eugenol, thymol, [114]

sanctum estragole

31 Basella alba Basellaceae Leaf High in vitamin A, vitamin C, Ca, [115]

Iron, phosphorus, vitamin B9 (folic
acid), calcium, magnesium, flavonoids,
polyphenols

32 Mentha Labiatae Leaf Flavonoids, acacetin, chrysoeriol,

arvensis diosmin, eriocitrin, hesperidin, luteolin,
esperidoside, menthoside, methyl
rosmarinate, rutin, tilianine, narirutin,
and nodifloretin. Phenolic acids such as
caffeic acid, lithospermic acid, rosmarinic
acid, protocatechuic acid, protocatechuic
aldehyde, phytosterols, β-sitosterol, and
daucosterol; the anthraquinones aloe-
emodin,emodin, chrysophanol, and tannins

33 Alternanthera Amaranthaceae Leaf Carotenoids, triterpene, saponins, [116]

sessilis flavonoids, steroids, stigmasterol,
β-sitosterol, glycosides, protein and amino
acids, campesterol, lupeol

34 Rumex acetosa Polygonaceae Leaf Oxalates, including calcium oxalate and [117]
tannins; anthracene derivatives, emodin,
rhein, quinoids, and flavonoids

35 Spinacia Amaranthaceae Leaf Vitamin A (especially high in lutein), [117]

oleracea vitamin C, vitamin E, vitamin K,
magnesium, manganese, folate, betaine,
iron, vitamin B2, calcium, potassium,
vitamin B6, folic acid, copper, protein,
phosphorus, zinc, niacin, selenium, and
omega-3 fatty acids. Recently, opioid
peptides called rubiscolins have also been
found in spinach. It is a source of folic acid

36 Trianthema Aizoaceae Tetraterpenoid 1 (trianthenol) flavonoid, [118–121]

portulacastrum 5,7-dihydroxy-6,8-dimethylchromone
(leptorumol) Isoamericanin A

37 Hibiscus Malvaceae Leaf Alkaloids, saponins, tannins, [122]

sabdariffa anthraquinones, cardiac glycosides,
flavonoids and phlobatannins

6. Conclusion

The most important free radical in biological systems is radical derivatives of

oxygen with the increasing acceptance of free radical as common place and impor-
tant biochemical intermediate. Antioxidants are believed to play a very important
role in the body defense system against reactive oxygen species (ROS), which are
the harmful by-products generated during normal cell aerobic respiration. The
imbalance between ROS and antioxidant defense system increases the oxidation

16
A Review on Natural Antioxidants
DOI: http://dx.doi.org/10.5772/intechopen.82636

burden and leads to the damage of macromolecules such as carbohydrates or

proteins, such processes of various diseases. To protect the cells and organ systems
of the body against reactive oxygen species, humans have evolved a highly sophis-
ticated and complex antioxidant protection system. Plants having vitamins (C, E,
carotenoids, etc.), flavonoids (flavones, isoflavones, flavanones, anthocyanins, and
catechins), polyphenols (ellagic acid, gallic acid, and tannins) possess remarkable
antioxidant activity. Antioxidant activity is neither restricted to a particular part
of plant nor the specific families. Current review reveals the different potential
application of antioxidant/free radical manipulations in prevention or control of
diseases. All plants discussed in this review exhibited significant, clinical, and
pharmacological activity with fewer side effects.

Author details

Arun Rasheed* and Rinshana Fathima Abdul Azeez

Department of Pharmaceutical Chemistry, Al Shifa College of Pharmacy,
Malappuram, Kerala, India

*Address all correspondence to: [email protected]

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms
of the Creative Commons Attribution License (http://creativecommons.org/licenses/
by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,
provided the original work is properly cited.

17
Traditional and Complementary Medicine

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