what properties of oxygen cause it to transform easily into a free radical

Pharmacogn Rev. 2010 Jul-Dec; iv(8): 118–126.

Free radicals, antioxidants and functional foods: Impact on human health

V. Lobo

Department of Phytology, Birla College, Kalyan – 421 304, Maharastra, Republic of india.

A. Patil

Department of Botany, Birla College, Kalyan – 421 304, Maharastra, Bharat.

A. Phatak

Section of Botany, Birla College, Kalyan – 421 304, Maharastra, India.

N. Chandra

Department of Phytology, Birla College, Kalyan – 421 304, Maharastra, India.

Received 2010 Mar 4; Revised 2010 Mar 8

Abstract

In recent years, there has been a great deal of attention toward the field of free radical chemical science. Complimentary radicals reactive oxygen species and reactive nitrogen species are generated by our body by diverse endogenous systems, exposure to different physiochemical conditions or pathological states. A balance betwixt free radicals and antioxidants is necessary for proper physiological part. If complimentary radicals overwhelm the body's power to regulate them, a condition known equally oxidative stress ensues. Gratis radicals thus adversely alter lipids, proteins, and Dna and trigger a number of human diseases. Hence awarding of external source of antioxidants can assist in coping this oxidative stress. Synthetic antioxidants such equally butylated hydroxytoluene and butylated hydroxyanisole take recently been reported to be dangerous for human health. Thus, the search for effective, nontoxic natural compounds with antioxidative activeness has been intensified in recent years. The present review provides a brief overview on oxidative stress mediated cellular damages and role of dietary antioxidants equally functional foods in the management of human diseases.

Keywords: Ageing, antioxidant, costless radicals, oxidative stress

INTRODUCTION

The recent growth in the knowledge of complimentary radicals and reactive oxygen species (ROS) in biology is producing a medical revolution that promises a new age of health and disease management.[1] It is ironic that oxygen, an element indispensable for life,[ii] under certain situations has deleterious effects on the human trunk.[3] Nigh of the potentially harmful furnishings of oxygen are due to the germination and activity of a number of chemical compounds, known as ROS, which take a tendency to donate oxygen to other substances. Free radicals and antioxidants take become ordinarily used terms in modernistic discussions of illness mechanisms.[four]

FREE RADICALS

A gratuitous radical tin be defined every bit whatever molecular species capable of independent existence that contains an unpaired electron in an diminutive orbital. The presence of an unpaired electron results in sure common properties that are shared by about radicals. Many radicals are unstable and highly reactive. They can either donate an electron to or have an electron from other molecules, therefore behaving as oxidants or reductants.[5] The most important oxygen-containing complimentary radicals in many disease states are hydroxyl radical, superoxide anion radical, hydrogen peroxide, oxygen singlet, hypochlorite, nitric oxide radical, and peroxynitrite radical. These are highly reactive species, capable in the nucleus, and in the membranes of cells of damaging biologically relevant molecules such equally Dna, proteins, carbohydrates, and lipids.[half-dozen] Free radicals attack important macromolecules leading to cell damage and homeostatic disruption. Targets of gratuitous radicals include all kinds of molecules in the trunk. Among them, lipids, nucleic acids, and proteins are the major targets.

Production of gratuitous radicals in the homo body

Costless radicals and other ROS are derived either from normal essential metabolic processes in the human torso or from external sources such equally exposure to 10-rays, ozone, cigarette smoking, air pollutants, and industrial chemicals.[3] Costless radical formation occurs continuously in the cells as a upshot of both enzymatic and nonenzymatic reactions. Enzymatic reactions, which serve as source of complimentary radicals, include those involved in the respiratory chain, in phagocytosis, in prostaglandin synthesis, and in the cytochrome P-450 system.[seven] Free radicals can too be formed in nonenzymatic reactions of oxygen with organic compounds besides as those initiated by ionizing reactions.

Some internally generated sources of free radicals are[8]

Mitochondria
Xanthine oxidase
Peroxisomes
Inflammation
Phagocytosis
Arachidonate pathways
Exercise
Ischemia/reperfusion injury
Some externally generated sources of free radicals are:
Cigarette smoke
Environmental pollutants
Radiation
Certain drugs, pesticides
Industrial solvents
Ozone

Costless radicals in biology

Free radical reactions are expected to produce progressive adverse changes that accrue with age throughout the torso [Tabular array 1]. Such "normal" changes with age are relatively mutual to all. Still, superimposed on this mutual pattern are patterns influenced by genetics and environmental differences that modulate gratuitous radical damage. These are manifested every bit diseases at certain ages adamant by genetic and ecology factors. Cancer and atherosclerosis, ii major causes of death, are salient "gratuitous radical" diseases. Cancer initiation and promotion is associated with chromosomal defects and oncogene activation. It is possible that endogenous free radical reactions, like those initiated by ionizing radiations, may consequence in tumor formation. The highly significant correlation between consumption of fats and oils and decease rates from leukemia and malignant neoplasia of the breast, ovaries, and rectum among persons over 55 years may be a reflection of greater lipid peroxidation.[ix] Studies on atherosclerosis reveal the probability that the disease may be due to costless radical reactions involving diet-derived lipids in the arterial wall and serum to yield peroxides and other substances. These compounds induce endothelial cell injury and produce changes in the arterial walls.[10]

Table 1

Free radicals[11–13]

An external file that holds a picture, illustration, etc. Object name is PRev-4-118-g001.jpg

CONCEPT OF OXIDATIVE STRESS

The term is used to draw the status of oxidative damage resulting when the critical balance between free radical generation and antioxidant defenses is unfavorable.[14] Oxidative stress, arising as a outcome of an imbalance between gratis radical product and antioxidant defenses, is associated with harm to a broad range of molecular species including lipids, proteins, and nucleic acids.[15] Short-term oxidative stress may occur in tissues injured past trauma, infection, heat injury, hypertoxia, toxins, and excessive exercise. These injured tissues produce increased radical generating enzymes (east.g., xanthine oxidase, lipogenase, cyclooxygenase) activation of phagocytes, release of gratuitous iron, copper ions, or a disruption of the electron send chains of oxidative phosphorylation, producing excess ROS. The initiation, promotion, and progression of cancer, besides as the side-effects of radiation and chemotherapy, have been linked to the imbalance between ROS and the antioxidant defense system. ROS take been implicated in the induction and complications of diabetes mellitus, historic period-related eye disease, and neurodegenerative diseases such as Parkinson'due south disease.[16]

Oxidative stress and human diseases

A function of oxidative stress has been postulated in many conditions, including anthersclerosis, inflammatory condition, sure cancers, and the process of aging. Oxidative stress is now thought to make a significant contribution to all inflammatory diseases (arthritis, vasculitis, glomerulonephritis, lupus erythematous, adult respiratory diseases syndrome), ischemic diseases (heart diseases, stroke, intestinal ischema), hemochromatosis, acquired immunodeficiency syndrome, emphysema, organ transplantation, gastric ulcers, hypertension and preeclampsia, neurological disorder (Alzheimer'south disease, Parkinson's affliction, muscular dystrophy), alcoholism, smoking-related diseases, and many others.[17] An excess of oxidative stress tin can lead to the oxidation of lipids and proteins, which is associated with changes in their construction and functions.

Cardiovascular diseases

Heart diseases continue to be the biggest killer, responsible for near half of all the deaths. The oxidative events may affect cardiovascular diseases therefore; it has potential to provide enormous benefits to the health and lifespan. Poly unsaturated fatty acids occur every bit a major role of the low density lipoproteins (LDL) in blood and oxidation of these lipid components in LDL play a vital function in atherosclerosis.[eighteen] The iii most important cell types in the vessel wall are endothelial cells; smooth muscle prison cell and macrophage can release free radical, which affect lipid peroxidation.[19] With continued high level of oxidized lipids, blood vessel harm to the reaction process continues and can atomic number 82 to generation of foam cells and plaque the symptoms of atherosclerosis. Oxidized LDL is antherogenic and is thought to be of import in the formation of anthersclerosis plaques. Furthermore, oxidized LDL is cytotoxic and can straight damage endothelial cells. Antioxidants similar B-carotene or vitamin E play a vital role in the prevention of diverse cardiovascular diseases.

Carcinogenesis

Reactive oxygen and nitrogen species, such equally super oxide anion, hydrogen peroxide, hydroxyl radical, and nitric oxide and their biological metabolites also play an important office in carcinogenesis. ROS induce Dna damage, as the reaction of complimentary radicals with Deoxyribonucleic acid includes strand break base modification and Deoxyribonucleic acid protein cantankerous-links. Numerous investigators have proposed participation of free radicals in carcinogenesis, mutation, and transformation; it is articulate that their presence in biosystem could atomic number 82 to mutation, transformation, and ultimately cancer. Consecration of mutagenesis, the all-time known of the biological upshot of radiation, occurs mainly through damage of Deoxyribonucleic acid by the HO. Radical and other species are produced past the radiolysis, and besides by direct radiations effect on Deoxyribonucleic acid, the reaction effects on DNA. The reaction of HO. Radicals is mainly addition to double bond of pyrimidine bases and abstraction of hydrogen from the sugar moiety resulting in chain reaction of DNA. These effects cause cell mutagenesis and carcinogenesis lipid peroxides are also responsible for the activation of carcinogens.

Antioxidants can decrease oxidative stress induced carcinogenesis past a direct scavenging of ROS and/or by inhibiting cell proliferation secondary to the poly peptide phosphorylation. B-carotene may exist protective confronting cancer through its antioxidant function, because oxidative products can cause genetic harm. Thus, the photo protective properties of B-carotene may protect against ultraviolet low-cal induced carcinogenesis. Immunoenhancement of B-carotene may contribute to cancer protection. B-carotene may as well take anticarcinogenic effect by altering the liver metabolism furnishings of carcinogens.[20] Vitamin C may be helpful in preventing cancer.[21] The possible mechanisms past which vitamin C may affect carcinogenesis include antioxidant effects, blocking of germination of nitrosanimes, enhancement of the immune response, and acceleration of detoxification of liver enzymes. Vitamin E, an important antioxidant, plays a role in immunocompetence by increasing humoral antibody protection, resistance to bacterial infections, prison cell-mediated immunity, the T-lymphocytes tumor necrosis factor product, inhibition of mutagen formation, repair of membranes in DNA, and blocking micro cell line formation.[22] Hence vitamin E may be useful in cancer prevention and inhibit carcinogenesis past the stimulation of the immune system. The administration of a mixture of the in a higher place three antioxidant reveled the highest reduction in risk of developing cardiac cancer.

Free radical and aging

The homo trunk is in constant battle to keep from aging. Research suggests that costless radical impairment to cells leads to the pathological changes associated with aging.[23] An increasing number of diseases or disorders, every bit well equally crumbling process itself, demonstrate link either direct or indirectly to these reactive and potentially destructive molecules.[24] The major mechanism of aging attributes to Dna or the accumulation of cellular and functional damage.[25] Reduction of costless radicals or decreasing their rate of production may delay crumbling. Some of the nutritional antioxidants will retard the aging process and foreclose disease. Based on these studies, it appears that increased oxidative stress ordinarily occurs during the crumbling process, and antioxidant status may significantly influence the effects of oxidative damage associated with advancing age. Research suggests that free radicals have a significant influence on aging, that free radical damage can exist controlled with adequate antioxidant defence, and that optimal intake of antioxidant nutrient may contribute to enhanced quality of life. Recent research indicates that antioxidant may even positively influence life span.

Oxidative damage to protein and Deoxyribonucleic acid

Oxidative harm to protein

Proteins can be oxidatively modified in three means: oxidative modification of specific amino acrid, free radical mediated peptide cleavage, and formation of protein cross-linkage due to reaction with lipid peroxidation products. Protein containing amino acids such equally methionine, cystein, arginine, and histidine seem to be the most vulnerable to oxidation.[26] Gratis radical mediated poly peptide modification increases susceptibility to enzyme proteolysis. Oxidative damage to poly peptide products may affect the activity of enzymes, receptors, and membrane ship. Oxidatively damaged protein products may contain very reactive groups that may contribute to harm to membrane and many cellular functions. Peroxyl radical is normally considered to be free radical species for the oxidation of proteins. ROS can damage proteins and produce carbonyls and other amino acids modification including formation of methionine sulfoxide and protein carbonyls and other amino acids modification including formation of methionine sulfoxide and poly peptide peroxide. Protein oxidation affects the alteration of bespeak transduction machinery, enzyme activeness, heat stability, and proteolysis susceptibility, which leads to aging.

Lipid peroxidation

Oxidative stress and oxidative modification of biomolecules are involved in a number of physiological and pathophysiological processes such as crumbling, artheroscleosis, inflammation and carcinogenesis, and drug toxicity. Lipid peroxidation is a free radical process involving a source of secondary complimentary radical, which further tin act as second messenger or can directly react with other biomolecule, enhancing biochemical lesions. Lipid peroxidation occurs on polysaturated fatty acid located on the jail cell membranes and it further proceeds with radical chain reaction. Hydroxyl radical is thought to initiate ROS and remove hydrogen atom, thus producing lipid radical and further converted into diene conjugate. Farther, by addition of oxygen it forms peroxyl radical; this highly reactive radical attacks another fatty acid forming lipid hydroperoxide (LOOH) and a new radical. Thus lipid peroxidation is propagated. Due to lipid peroxidation, a number of compounds are formed, for instance, alkanes, malanoaldehyde, and isoprotanes. These compounds are used equally markers in lipid peroxidation assay and accept been verified in many diseases such as neurogenerative diseases, ischemic reperfusion injury, and diabetes.[27]

Oxidative damage to Dna

Many experiments conspicuously provide evidences that DNA and RNA are susceptible to oxidative harm. It has been reported that particularly in crumbling and cancer, DNA is considered every bit a major target.[28] Oxidative nucleotide as glycol, dTG, and 8-hydroxy-ii-deoxyguanosine is plant to be increased during oxidative damage to DNA under UV radiation or free radical damage. It has been reported that mitochondrial DNA are more susceptible to oxidative harm that have office in many diseases including cancer. It has been suggested that 8-hydroxy-2-deoxyguanosine can be used as biological marker for oxidative stress.[29]

ANTIOXIDANTS

An antioxidant is a molecule stable enough to donate an electron to a rampaging free radical and neutralize information technology, thus reducing its capacity to harm. These antioxidants delay or inhibit cellular damage mainly through their free radical scavenging property.[30] These depression-molecular-weight antioxidants tin safely interact with free radicals and terminate the chain reaction before vital molecules are damaged. Some of such antioxidants, including glutathione, ubiquinol, and uric acid, are produced during normal metabolism in the torso.[31] Other lighter antioxidants are found in the diet. Although there are several enzymes arrangement within the body that scavenge gratis radicals, the principle micronutrient (vitamins) antioxidants are vitamin Due east (α-tocopherol), vitamin C (ascorbic acid), and B-carotene.[32] The body cannot manufacture these micronutrients, then they must be supplied in the diet.

History

The term antioxidant originally was used to refer specifically to a chemical that prevented the consumption of oxygen. In the late 19th and early 20th century, extensive report was devoted to the uses of antioxidants in important industrial processes, such every bit the prevention of metal corrosion, the vulcanization of safe, and the polymerization of fuels in the fouling of internal combustion engines.[33]

Early research on the role of antioxidants in biology focused on their use in preventing the oxidation of unsaturated fats, which is the cause of rancidity.[34] Antioxidant action could exist measured simply by placing the fat in a airtight container with oxygen and measuring the charge per unit of oxygen consumption. Yet, it was the identification of vitamins A, C, and E as antioxidants that revolutionized the field and led to the realization of the importance of antioxidants in the biochemistry of living organisms.[35,36] The possible mechanisms of activity of antioxidants were beginning explored when it was recognized that a substance with antioxidative activity is likely to be one that is itself readily oxidized.[37] Research into how vitamin East prevents the process of lipid peroxidation led to the identification of antioxidants as reducing agents that prevent oxidative reactions, often by scavenging ROS before they can damage cells.[38]

Antioxidant defense arrangement

Antioxidants act as radical scavenger, hydrogen donor, electron donor, peroxide decomposer, singlet oxygen quencher, enzyme inhibitor, synergist, and metallic-chelating agents. Both enzymatic and nonenzymatic antioxidants be in the intracellular and extracellular surround to detoxify ROS.[39]

Mechanism of action of antioxidants

Two principle mechanisms of action have been proposed for antioxidants.[40] The kickoff is a chain- breaking mechanism by which the primary antioxidant donates an electron to the free radical present in the systems. The 2d mechanism involves removal of ROS/reactive nitrogen species initiators (secondary antioxidants) by quenching concatenation-initiating catalyst. Antioxidants may exert their upshot on biological systems past different mechanisms including electron donation, metal ion chelation, co-antioxidants, or by factor expression regulation.[41]

Levels of antioxidant activeness

The antioxidants acting in the defense systems human action at different levels such equally preventive, radical scavenging, repair and de novo, and the 4th line of defence force, i.e., the adaptation.

The first line of defence force is the preventive antioxidants, which suppress the formation of free radicals. Although the precise mechanism and site of radical formation in vivo are not well elucidated yet, the metal-induced decompositions of hydroperoxides and hydrogen peroxide must be one of the important sources. To suppress such reactions, some antioxidants reduce hydroperoxides and hydrogen peroxide beforehand to alcohols and h2o, respectively, without generation of complimentary radicals and some proteins sequester metallic ions.

Glutathione peroxidase, glutathione-s-transferase, phospholipid hydroperoxide glutathione peroxidase (PHGPX), and peroxidase are known to decompose lipid hydroperoxides to respective alcohols. PHGPX is unique in that it tin reduce hydroperoxides of phospholipids integrated into biomembranes. Glutathione peroxidase and catalase reduce hydrogen peroxide to water.

The second line of defense is the antioxidants that scavenge the active radicals to suppress chain initiation and/or break the chain propagation reactions. Diverse endogenous radical-scavenging antioxidants are known: some are hydrophilic and others are lipophilic. Vitamin C, uric acid, bilirubin, albumin, and thiols are hydrophilic, radical-scavenging antioxidants, while vitamin E and ubiquinol are lipophilic radical-scavenging antioxidants. Vitamin E is accepted as the well-nigh potent radical-scavenging lipophilic antioxidant.

The third line of defense is the repair and de novo antioxidants. The proteolytic enzymes, proteinases, proteases, and peptidases, present in the cytosol and in the mitochondria of mammalian cells, recognize, degrade, and remove oxidatively modified proteins and prevent the aggregating of oxidized proteins.

The Dna repair systems also play an of import part in the total defense system against oxidative damage. Diverse kinds of enzymes such as glycosylases and nucleases, which repair the damaged Deoxyribonucleic acid, are known.

At that place is another important role called accommodation where the signal for the product and reactions of free radicals induces formation and transport of the appropriate antioxidant to the correct site.[42]

ENZYMATIC

Types of antioxidants

Cells are protected confronting oxidative stress by an interacting network of antioxidant enzymes.[43] Here, the superoxide released by processes such equally oxidative phosphorylation is commencement converted to hydrogen peroxide so further reduced to give water. This detoxification pathway is the result of multiple enzymes, with superoxide dismutases catalyzing the offset step and then catalases and various peroxidases removing hydrogen peroxide.[44]

Superoxide dismutase

Superoxide dismutases (SODs) are a form of closely related enzymes that catalyze the breakdown of the superoxide anion into oxygen and hydrogen peroxide.[45,46] SOD enzymes are present in most all aerobic cells and in extracellular fluids.[47] At that place are three major families of superoxide dismutase, depending on the metal cofactor: Cu/Zn (which binds both copper and zinc), Fe and Mn types (which bind either iron or manganese), and finally the Ni type which binds nickel.[48] In higher plants, SOD isozymes take been localized in dissimilar cell compartments. Mn-SOD is present in mitochondria and peroxisomes. Fe-SOD has been institute mainly in chloroplasts but has also been detected in peroxisomes, and CuZn-SOD has been localized in cytosol, chloroplasts, peroxisomes, and apoplast.[48–50]

In humans (every bit in all other mammals and most chordates), 3 forms of superoxide dismutase are nowadays. SOD1 is located in the cytoplasm, SOD2 in the mitochondria, and SOD3 is extracellular. The first is a dimer (consists of two units), while the others are tetramers (four subunits). SOD1 and SOD3 contain copper and zinc, while SOD2 has manganese in its reactive heart.[51]

Catalase

Catalase is a mutual enzyme institute in near all living organisms, which are exposed to oxygen, where information technology functions to catalyze the decomposition of hydrogen peroxide to water and oxygen.[52] Hydrogen peroxide is a harmful by-product of many normal metabolic processes: to forestall impairment, it must be quickly converted into other, less dangerous substances. To this end, catalase is frequently used by cells to rapidly catalyze the decomposition of hydrogen peroxide into less reactive gaseous oxygen and water molecules.[53] All known animals utilise catalase in every organ, with particularly high concentrations occurring in the liver.[54]

Glutathione systems

The glutathione organisation includes glutathione, glutathione reductase, glutathione peroxidases, and glutathione South-transferases. This arrangement is institute in animals, plants, and microorganisms.[55] Glutathione peroxidase is an enzyme containing 4 selenium-cofactors that catalyze the breakdown of hydrogen peroxide and organic hydroperoxides. There are at least iv different glutathione peroxidase isozymes in animals.[56] Glutathione peroxidase one is the virtually abundant and is a very efficient scavenger of hydrogen peroxide, while glutathione peroxidase iv is most active with lipid hydroperoxides. The glutathione Southward-transferases show high activeness with lipid peroxides. These enzymes are at specially high levels in the liver and also serve in detoxification metabolism.[57]

NONENZYMATIC

Ascorbic acid

Ascorbic acid or "vitamin C" is a monosaccharide antioxidantfound in both animals and plants. As it cannot be synthesized in humans and must be obtained from the diet, it is a vitamin.[58] Most other animals are able to produce this compound in their bodies and do not crave it in their diets. In cells, it is maintained in its reduced form past reaction with glutathione, which can exist catalyzed past protein disulfide isomerase and glutaredoxins.[59] Ascorbic acid is a reducing agent and can reduce and thereby neutralize ROS such as hydrogen peroxide.[lx] In addition to its straight antioxidant effects, ascorbic acid is also a substrate for the antioxidant enzyme ascorbate peroxidase, a function that is particularly important in stress resistance in plants.[61]

Glutathione

Glutathione is a cysteine-containing peptide found in mostforms of aerobic life.[62] Information technology is not required in the diet and is instead synthesized in cells from its elective amino acids. Glutathione has antioxidant properties since the thiol grouping in its cysteine moiety is a reducing agent and can be reversibly oxidized and reduced. In cells, glutathione is maintained in the reduced class by the enzyme glutathione reductase and in turn reduces other metabolites and enzyme systems as well equally reacting straight with oxidants.[63] Due to its high concentration and cardinal office in maintaining the cell's redox state, glutathione is one of the most important cellular antioxidants.[33] In some organisms, glutathione is replaced past other thiols, such as by mycothiol in the actinomycetes, or by trypanothione in the kinetoplastids.[64]

Melatonin

Melatonin, also known chemically as N-acetyl-5-methoxytryptamine,[65] is a naturally occurring hormone plant in animals and in some other living organisms, including algae.[66] Melatonin is a powerful antioxidant that tin easily cross prison cell membranes and the blood–brain barrier.[67] Unlike other antioxidants, melatonin does not undergo redox cycling, which is the ability of a molecule to undergo repeated reduction and oxidation. Melatonin, once oxidized, cannot be reduced to its onetime state because information technology forms several stable cease-products upon reacting with free radicals. Therefore, it has been referred to every bit a terminal (or suicidal) antioxidant.[68]

Tocopherols and tocotrienols (Vitamin E)

Vitamin E is the commonage proper name for a gear up of eight related tocopherols and tocotrienols, which are fat-soluble vitamins with antioxidant properties.[69] Of these, α-tocopherol has been near studied every bit it has the highest bioavailability, with the body preferentially absorbing and metabolizing this form.[70] It has been claimed that the α-tocopherol form is the most important lipid-soluble antioxidant, and that it protects membranes from oxidation by reacting with lipid radicals produced in the lipid peroxidation chain reaction.[71] This removes the free radical intermediates and prevents the propagation reaction from standing. This reaction produces oxidized α-tocopheroxyl radicals that can exist recycled back to the active reduced class through reduction past other antioxidants, such as ascorbate, retinol, or ubiquinol.[72]

Uric acid

Uric acrid accounts for roughly one-half the antioxidant ability of plasma. In fact, uric acrid may have substituted for ascorbate in man evolution.[73] Yet, similar ascorbate, uric acrid can also mediate the production of active oxygen species.

PLANTS AS SOURCE OF ANTIOXIDANTS

Constructed and natural nutrient antioxidants are used routinely in foods and medicine especially those containing oils and fats to protect the nutrient against oxidation. There are a number of constructed phenolic antioxidants, butylated hydroxytoluene (BHT) and butylated hydroxyanisole (BHA) existence prominent examples. These compounds have been widely uses as antioxidants in nutrient industry, cosmetics, and therapeutic industry. However, some physical properties of BHT and BHA such every bit their high volatility and instability at elevated temperature, strict legislation on the use of synthetic nutrient additives, carcinogenic nature of some synthetic antioxidants, and consumer preferences take shifted the attending of manufacturers from synthetic to natural antioxidants.[74] In view of increasing hazard factors of human to various deadly diseases, there has been a global tendency toward the use of natural substance nowadays in medicinal plants and dietary plats as therapeutic antioxidants. It has been reported that there is an inverse human relationship between the dietary intake of antioxidant-rich food and medicinal plants and incidence of human diseases. The utilize of natural antioxidants in food, cosmetic, and therapeutic manufacture would be promising culling for constructed antioxidants in respect of low cost, highly uniform with dietary intake and no harmful effects inside the human body. Many antioxidant compounds, naturally occurring in plant sources accept been identified as complimentary radical or active oxygen scavengers.[75] Attempts have been made to report the antioxidant potential of a broad variety of vegetables like potato, spinach, tomatoes, and legumes.[76] There are several reports showing antioxidant potential of fruits.[77] Strong antioxidants activities have been constitute in berries, cherries, citrus, prunes, and olives. Green and blackness teas have been extensively studied in the recent past for antioxidant properties since they comprise up to 30% of the dry out weight as phenolic compounds.[78]

Apart from the dietary sources, Indian medicinal plants as well provide antioxidants and these include (with common/ayurvedic names in brackets) Acacia catechu (kair), Aegle marmelos (Bengal quince, Bel), Allium cepa (Onion), A. sativum (Garlic, Lahasuna), Aleo vera (Indain aloe, Ghritkumari), Amomum subulatum (Greater cardamom, Bari elachi), Andrographis paniculata (Kiryat), Asparagus recemosus (Shatavari), Azadirachta indica (Neem, Nimba), Bacopa monniera (Brahmi), Butea monosperma (Palas, Dhak), Camellia sinensis (Dark-green tea), Cinnamomum verum (Cinnamon), Cinnamomum tamala (Tejpat), Curcma longa (Turmeric, Haridra), Emblica officinalis (Inhian gooseberry, Amlaki), Glycyrrhiza glapra (Yashtimudhu), Hemidesmus indicus (Indian Sarasparilla, Anantamul), Indigofera tinctoria, Mangifera indica (Mango, Amra), Momordica charantia (Bitter gourd), Murraya koenigii (Curry leafage), Nigella sativa (Black cumin), Ocimum sanctum (Holy basil, Tusil), Onosma echioides (Ratanjyot), Picrorrhiza kurroa (Katuka), Piper beetle, Plumbago zeylancia (Chitrak), Sesamum indicum, Sida cordifolia,Spirulina fusiformis (Alga), Swertia decursata, Syzigium cumini (Jamun), Terminalia ariuna (Arjun), Terminalia bellarica (Beheda), Tinospora cordifolia (Heart leaved moonseed, Guduchi), Trigonella foenum-graecium (Fenugreek), Withania somifera (Winter cherry, Ashwangandha), and Zingiber officinalis (Ginger).[79]

ANTIOXIDANT POTENTIAL OF INDIAN FUNCTIONAL FOODS

Concepts of functional foods and nutraceuticals

In the last decade, preventive medicine has undergone a great advance, especially in adult countries. Research has demonstrated that nutrition plays a crucial role in the prevention of chronic diseases, as most of them can exist related to nutrition. Functional food enters the concept of considering food not only necessary for living but also as a source of mental and physical well-being, contributing to the prevention and reduction of gamble factors for several diseases or enhancing sure physiological functions.[eighty] A food can exist regarded as functional if it is satisfactorily demonstrated to bear on beneficially 1 or more target functions in the torso, across adequate nutritional effects, in a fashion which is relevant to either the country of well being and health or reduction of the risk of a disease. The beneficial effects could be either maintenance or promotion of a state of well beingness or health and/or a reduction of risk of a pathologic process or a affliction.[81] Whole foods represent the simplest example of functional food. Broccoli, carrots, and tomatoes are considered functional foods because of their high contents of physiologically active components (sulforaphen, B-carotene, and lycopene, respectively). Light-green vegetables and spices like mustard and turmeric, used extensively in Indian cuisine, also can fall under this category.[82] "Nutraceutical" is a term coined in 1979 by Stephen DeFelice.[83] Information technology is defined "as a food or parts of nutrient that provide medical or health benefits, including the prevention and treatment of disease." Nutraceuticals may range from isolated nutrients, dietary supplements, and diets to genetically engineered "designer" food, herbal products, and processed products such every bit cereals, soups, and beverages. A nutraceutical is whatever nontoxic food excerpt supplement that has scientifically proven health benefits for both the handling and prevention of disease.[84] The increasing involvement in nutraceuticals reflects the fact that consumers hear about epidemiological studies indicating that a specific diet or component of the diet is associated with a lower risk for a certain disease. The major agile nutraceutical ingredients in plants are flavonoids. Every bit is typical for phenolic compounds, they can act as potent antioxidants and metal chelators. They likewise accept long been recognized to possess anti-inflammatory, antiallergic, hepatoprotective, antithrombotic, antiviral, and anticarcinogenic activities.[85]

Indian dietary and medicinal plants every bit functional foods

Ingredients that brand food functional are dietary fibers, vitamins, minerals, antioxidants, oligosaccharides, essential fat acids (omega-three), lactic acid bacteria cultures, and lignins. Many of these are present in medicinal plants. Indian systems of medicine believe that complex diseases tin be treated with complex combination of botanicals unlike in west, with single drugs. Whole foods are hence used in Bharat equally functional foods rather than supplements. Some medicinal plants and dietary constituents having functional attributes are spices such as onion, garlic, mustard, ruby-red chilies, turmeric, clove, cinnamon, saffron, curry leaf, fenugreek, and ginger. Some herbs as Bixa orellana and vegetables like amla, wheat grass, soyabean, and Gracinia cambogia have antitumor effects. Other medicinal plants with functional properties include A.marmelos, A. cepa, Aloe vera, A. paniculata, Azadirachta bharat, and Brassica juncea.[86]

CONCLUSION

Gratis radicals damage contributes to the etiology of many chronic wellness issues such as cardiovascular and inflammatory disease, cataract, and cancer. Antioxidants prevent free radical induced tissue damage by preventing the germination of radicals, scavenging them, or by promoting their decomposition. Synthetic antioxidants are recently reported to be dangerous to human health. Thus the search for effective, nontoxic natural compounds with antioxidative activity has been intensified in contempo years. In addition to endogenous antioxidant defense force systems, consumption of dietary and establish-derived antioxidants appears to be a suitable culling. Dietary and other components of plants course a major source of antioxidants. The traditional Indian nutrition, spices, and medicinal plants are rich sources of natural antioxidants; higher intake of foods with functional attributes including high level of antioxidants in antioxidants in functional foods is one strategy that is gaining importance.

Newer approaches utilizing collaborative inquiry and modern technology in combination with established traditional health principles volition yield dividends in near future in improving health, peculiarly amongst people who practice not accept access to the utilise of costlier western systems of medicine.

Footnotes

Source of Support: Nil

Conflict of Interest: None declared

REFERENCES

1. Aruoma OI. Methodological consideration for characterization for potential antioxidant actions of bioactive components in plants foods. Mutat Res. 2003;532:9–20. [PubMed] [Google Scholar]

2. Mohammed AA, Ibrahim AA. Pathological roles of reactive oxygen species and their defence force machinery. Saudi Pharm J. 2004;12:one–18. [Google Scholar]

three. Bagchi G, Puri Southward. Free radicals and antioxidants in health and disease. Due east Mediterranean Health Jr. 1998;4:350–60. [Google Scholar]

iv. Aruoma OI. Nutrition and wellness aspects of complimentary radicals and antioxidants. Nutrient Chem Toxicol. 1994;32:671–83. [PubMed] [Google Scholar]

5. Cheeseman KH, Slater TF. An introduction to complimentary radicals chemistry. Br Med Balderdash. 1993;49:481–93. [PubMed] [Google Scholar]

7. Liu T, Stern A, Roberts LJ. The isoprostanes: Novel prostanglandin-like products of the costless radical catalyzed peroxidation of arachidonic acid. J Biomed Sci. 1999;6:226–35. [PubMed] [Google Scholar]

8. Ebadi M. Antioxidants and costless radicals in health and disease: An introduction to reactive oxygen species, oxidative injury, neuronal jail cell death and therapy in neurodegenerative diseases. Arizona: Prominent Press; 2001. [Google Scholar]

9. Lea AJ. Dietary factors associated with expiry rates from certain neoplasms in man. Lancet. 1966;two:332–3. [PubMed] [Google Scholar]

ten. Harman D. Role of free radicals in crumbling and disease. Ann N Y Acad Sci. 1992;673:126–41. [PubMed] [Google Scholar]

11. Sies H. Oxidative stress: Introductory remarks. In: Sies H, editor. Oxidative Stress. San Diego: Bookish Press; 1985. pp. ane–7. [Google Scholar]

12. Docampo R. Antioxidant mechanisms. In: Marr J, Müller M, editors. Biochemistry and Molecular Biological science of Parasites. London: Academic Press; 1995. pp. 147–60. [Google Scholar]

13. Rice-Evans CA, Gopinathan V. Oxygen toxicity, free radicals and antioxidants in homo disease: Biochemical implications in atherosclerosis and the issues of premature neonates. Essays Biochem. 1995;29:39–63. [PubMed] [Google Scholar]

14. Rock CL, Jacob RA, Bowen PE. Update o biological characteristics of the antioxidant micronutrients- Vitamin C, Vitamin E and the carotenoids. J Am Diet Assoc. 1996;96:693–702. [PubMed] [Google Scholar]

15. Mc Cord JM. The evolution of complimentary radicals and oxidative stress. Am J Med. 2000;108:652–9. [PubMed] [Google Scholar]

16. Rao AL, Bharani Chiliad, Pallavi V. Function of antioxidants and free radicals in health and disease. Adv Pharmacol Toxicol. 2006;vii:29–38. [Google Scholar]

17. Stefanis 50, Burke RE, Greene LA. Apoptosis in neurodegenerative disorders. Curr Opin Neurol. 1997;10:299–305. [PubMed] [Google Scholar]

18. Esterbauer H, Pubi H, Dieber-Rothender M. Outcome of antioxidants on oxidative modification of LDL. Ann Med. 1991;23:573–81. [PubMed] [Google Scholar]

19. Neuzil J, Thomas SR, Stocker R. Requirement for promotion, or inhibition of α- tocopherol of radical induced initiation of plasma lipoprotein lipid peroxidation. Costless Radic Biol Med. 1997;22:57–71. [PubMed] [Google Scholar]

20. Poppel GV, Golddbohm RA. Epidemiologic evidence for β – carotene and cancer prevention. Am J Clin Nutr. 1995;62:1393–5. [PubMed] [Google Scholar]

21. Glatthaar Exist, Horing DH, Moser U. The role of ascorbic acrid in carcinogenesis. Adv Exp Med Biol. 1986;206:357–77. [PubMed] [Google Scholar]

22. Sokol RJ. Vitamin E deficiency and neurologic diseses. Annu Rev Nutr. 1988;8:351–73. [PubMed] [Google Scholar]

23. Ashok BT, Ali R. The aging paradox: Free radical theory of crumbling. Exp Gerontol. 1999;34:293–303. [PubMed] [Google Scholar]

24. Sastre J, Pellardo FV, Vina J. Glutathione, oxidative stress and aging. Age. 1996;19:129–39. [Google Scholar]

25. Cantuti-Castelvetri I, Shukitt-Hale B, Joseph JA. Neurobehavioral aspects of antioxidants in aging. Int J Dev Neurosci. 2000;eighteen:367–81. [PubMed] [Google Scholar]

26. Freeman BA, Crapo JD. Biology of disease: Free radicals and tissue injury. Lab Invest. 1982;47:412–26. [PubMed] [Google Scholar]

27. Lovell MA, Ehmann WD, Buffer BM, Markesberry WR. Elevated thiobarbituric acrid reactive substances and antioxidant enzyme activity in the encephalon in Alzemers disease. Neurology. 1995;45:1594–601. [PubMed] [Google Scholar]

28. Woo RA, Melure KG, Lee PW. DNA dependent protein kinase acts upstream of p53 in response to DNA impairment. Nature. 1998;394:700–4. [PubMed] [Google Scholar]

29. Hattori Y, Nishigori C, Tanaka T, Ushida 1000, Nikaido O, Osawa T. 8 Hydroxy-2-deoxyguanosine is increased in epidermal cells of hairless mice afterward chronic ultraviolet B exposure. J Invest Dermatol. 1997;89:10405–nine. [PubMed] [Google Scholar]

30. Halliwell B. How to narrate an antioxidant- An update. Biochem Soc Symp. 1995;61:73–101. [PubMed] [Google Scholar]

31. Shi HL, Noguchi N, Niki N. Comparative written report on dynamics of antioxidative activity of α- tocopheryl hydroquinone, ubiquinol and α- tocopherol, against lipid peroxidation. Free Radic Biol Med. 1999;27:334–46. [PubMed] [Google Scholar]

32. Levine One thousand, Ramsey SC, Daruwara R. Criteria and recommendation for Vitamin C intake. JAMA. 1991;281:1415–23. [PubMed] [Google Scholar]

33. Matill HA. Antioxidants. Annu Rev Biochem. 1947;16:177–92. [PubMed] [Google Scholar]

34. German J. Nutrient processing and lipid oxidation. Adv Exp Med Biol. 1999;459:23–50. [PubMed] [Google Scholar]

35. Jacob R. Three eras of vitamin C discovery. Subcell Biochem. 1996;25:1–16. [PubMed] [Google Scholar]

36. Knight J. Free radicals: Their history and current status in aging and illness. Ann Clin Lab Sci. 1998;28:331–46. [PubMed] [Google Scholar]

37. Moreau, Dufraisse Comptes Rendus des Séances et Mémoires de la Société de Biologie. 1922;86:321. [Google Scholar]

38. Wolf G. The discovery of the antioxidant part of vitamin E: The contribution of Henry A. Mattill. J Nutr. 2005;135:363–vi. [PubMed] [Google Scholar]

39. Frie B, Stocker R, Ames BN. Antioxidant defences and lipid peroxidation in homo blood plasma. Proc Natl Acad Sci. 1988;37:569–71. [Google Scholar]

40. Rice-Evans CA, Diplock AT. Current status of antioxidant therapy. Costless Radic Biol Med. 1993;15:77–96. [PubMed] [Google Scholar]

41. Krinsky NI. Machinery of activeness of biological antioxidants. Proc Soc Exp Biol Med. 1992;200:248–54. [PubMed] [Google Scholar]

42. Niki Eastward. Antioxidant defenses in eukaryotic cells. In: Poli Grand, Albano E, Dianzani MU, editors. Gratis radicals: From bones science to medicine. Basel, Switzerland: Birkhauser Verlag; 1993. pp. 365–73. [Google Scholar]

43. Sies H. Oxidative stress: Oxidants and antioxidants. Exp Physiol. 1997;82:291–5. [PubMed] [Google Scholar]

44. Magnenat JL, Garganoam M, Cao J. The nature of antioxidant defense mechanisms: A lesson from transgenic studies. Environ Health Perspect. 1998;106:1219–28. [PMC gratuitous article] [PubMed] [Google Scholar]

45. Zelko I, Mariani T, Folz R. Superoxide dismutase multigene family: A comparison of the CuZn-SOD (SOD1), Mn-SOD (SOD2), and EC-SOD (SOD3) gene structures, evolution, and expression. Free Radic Biol Med. 2002;33:337–49. [PubMed] [Google Scholar]

46. Banniste J, Bannister Westward, Rotilio G. Aspects of the structure, function, and applications of superoxide dismutase. CRC Crit Rev Biochem. 1987;22:111–80. [PubMed] [Google Scholar]

47. Johnson F, Giulivi C. Superoxide dismutases and their impact upon human health. Mol Aspects Med. 2005;26:340–52. [PubMed] [Google Scholar]

48. Wuerges J, Lee JW, Yim YI, Yim HS, Kang SO, Djinovic Carugo Yard. Crystal construction of nickel-containing superoxide dismutase reveals another blazon of agile site. Proc Natl Acad Sci. 2004;101:8569–74. [PMC free article] [PubMed] [Google Scholar]

49. Corpas FJ, Barroso JB, del Río LA. Peroxisomes as a source of reactive oxygen species and nitric oxide point molecules in plant cells. Trends Plant Sci. 2001;vi:145–50. [PubMed] [Google Scholar]

l. Corpas FJ, Fernández-Ocaña A, Carreras A, Valderrama R, Luque F, Esteban FJ, et al. The expression of different superoxide dismutase forms is cell-type dependent in olive (Olea europaea L.) leaves. Institute Cell Physiol. 2006;47:984–94. [PubMed] [Google Scholar]

51. Cao X, Antonyuk SV, Seetharaman SV, Whitson LJ, Taylor AB, Holloway SP, et al. Structures of the G85R variant of SOD1 in familial amyotrophic lateral sclerosis. J Biol Chem. 2008;283:16169–77. [PMC free article] [PubMed] [Google Scholar]

52. Chelikani P, Fita I, Loewen PC. Multifariousness of structures and properties among catalases. Cell Mol Life Sci. 2004;61:192–208. [PubMed] [Google Scholar]

53. Gaetani Yard, Ferraris A, Rolfo K, Mangerini R, Arena Due south, Kirkman H. Predominant role of catalase in the disposal of hydrogen peroxide within human erythrocytes. Blood. 1996;87:1595–9. [PubMed] [Google Scholar]

54. Eisner T, Aneshansley DJ. Spray aiming in the bombardier beetle: Photographic bear witness. Proc Natl Acad Sci USA. 1999;96:9705–9. [PMC gratuitous article] [PubMed] [Google Scholar]

55. Meister A, Anderson G. Glutathione. Annu Rev Biochem. 1983;52:711–sixty. [PubMed] [Google Scholar]

56. Brigelius-Flohe R. Tissue-specific functions of individual glutathione peroxidases. Gratuitous Radic Biol Med. 1999;27:951–65. [PubMed] [Google Scholar]

57. Hayes J, Flanagan J, Jowsey I. Glutathione transferases. Annu Rev Pharmacol Toxicol. 2005;45:51–88. [PubMed] [Google Scholar]

58. Smirnoff Northward. L-ascorbicacid biosynthesis. Vitam Horm. 2001;61:241–66. [PubMed] [Google Scholar]

59. Meister A. Glutathione-ascorbic acid antioxidant system in animals. J Biol Chem. 1994;269:9397–400. [PubMed] [Google Scholar]

60. Padayatty Due south, Katz A, Wang Y, Eck P, Kwon O, Lee J, et al. Vitamin C equally an antioxidant: Evaluation of its role in disease prevention. J Am Coll Nutr. 2003;22:18–35. [PubMed] [Google Scholar]

61. Shigeoka S, Ishikawa T, Tamoi One thousand, Miyagawa Y, Takeda T, Yabuta Y, et al. Regulation and role of ascorbate peroxidase isoenzymes. J Exp Bot. 2002;53:1305–19. [PubMed] [Google Scholar]

62. Meister A, Anderson A. Glutathione. Annu Rev Biochem. 1983;52:711–60. [PubMed] [Google Scholar]

63. Meister A. Glutathione metabolism and its selective modification. J Biol Chem. 1988;263:17205–eight. [PubMed] [Google Scholar]

64. Fairlamb AH, Cerami A. Metabolism and functions of trypanothione in the Kinetoplastida. Annu Rev Microbiol. 1992;46:695–729. [PubMed] [Google Scholar]

65. Nassar Eastward, Mulligan C, Taylor L, Kerksick C, Galbreath One thousand, Greenwood M, et al. Effects of a unmarried dose of N-Acetyl-v-methoxytryptamine (Melatonin) and resistance exercise on the growth hormone/IGF-1 axis in immature males and females. J Int Soc Sports Nutr. 2007;4:14. [PMC free commodity] [PubMed] [Google Scholar]

66. Caniato R, Filippini R, Piovan A, Puricelli L, Borsarini A, Cappelletti E. Melatonin in plants. Adv Exp Med Biol. 2003;527:593–7. [PubMed] [Google Scholar]

67. Reiter RJ, Carneiro RC, Oh CS. Melatonin in relation to cellular antioxidative defence force mechanisms. Horm Metab Res. 1997;29:363–72. [PubMed] [Google Scholar]

68. Tan DX, Manchester LC, Reiter RJ, Qi WB, Karbownik M, Calvo JR. Significance of melatonin in antioxidative defense system: Reactions and products. Biol Signals Recept. 2000;9:137–59. [PubMed] [Google Scholar]

69. Herrera Due east, Barbas C. Vitamin Due east: Action, metabolism and perspectives. J Physiol Biochem. 2001;57:43–56. [PubMed] [Google Scholar]

70. Brigelius-Flohe R, Traber M. Vitamin Eastward: Function and metabolism. FASEB J. 1999;thirteen:1145–55. [PubMed] [Google Scholar]

71. Traber MG, Atkinson J. Vitamin E, antioxidant and zero more than. Free Radic Biol Med. 2007;43:4–15. [PMC complimentary article] [PubMed] [Google Scholar]

72. Wang X, Quinn P. Vitamin East and its function in membranes. Prog Lipid Res. 1999;38:309–36. [PubMed] [Google Scholar]

73. Jaeschke H, Gores GJ, Cederbaum AI, Hinson JA, Pessayre D, Lemasters JJ. Mechanisms of hepatotoxicity. Toxicol Sci. 2002;65:166–76. [PubMed] [Google Scholar]

74. Papas AM. Nutrition and antioxidant status. Nutrient Chem Toxicol. 1999;37:999–1007. [PubMed] [Google Scholar]

75. Brown JE, Rice-Evan CA. Luteolin-rich Artichoke extract protects low density lipoprotein from oxidation in vitro. Costless Radic Res. 1998;29:247–255. [PubMed] [Google Scholar]

76. Furuta S, Nishiba Y, Suda I. Fluorometric assay for screening antioxidative activities of vegetables. J Food Sci. 1997;62:526–8. [Google Scholar]

77. Wang H, Cao G, Prior RL. Total antioxidant capacity of fruits. J Agric Food Chem. 1996;44:701–5. [Google Scholar]

78. Lin JK, Lin CH, Ling YC, Lin-Shian SY, Juan IM. Survey of catechins, gallic acid and methylxantines in green, oolong, puerh and blackness teas. J Agric Food Chem. 1998;46:3635–42. [Google Scholar]

79. Devasagayam TP, Tilak JC, Boloor KK, Sane KS, Ghaskadbi SS, Lele RD. Free radicals and antioxidants in Human Health: Current condition and time to come prospects. J Assoc Physicians Bharat. 2004;52:794–803. [PubMed] [Google Scholar]

80. López-Varela S, González-Gross M, Marcos A. Functional foods and the immune system: A review. Eur J Clin Nutr. 2002;56:S29–33. [PubMed] [Google Scholar]

81. Roberfroid MB. What is beneficial for wellness? The concept of functional food. Nutrient Chem Toxicol. 1999;37:1034–41. [PubMed] [Google Scholar]

82. Krishnaswamy K. Indian functional food: Role in prevention of cancer. Nutr Rev. 1996;54:127–31. [PubMed] [Google Scholar]

83. DeFelice SL. Nutraceuticals: Opportunities in an Emerging Marketplace. Scrip Mag. 1992;nine:14–five. [Google Scholar]

84. Dillard CJ, German language JB. Phytochemicals: Nutraceuticals and homo health. J Sci Food Agric. 2000;fourscore:1744–56. [Google Scholar]

85. Tapas AR, Sakarkar DM, Kakde RB. Review article flavonoids as nutraceuticals: A review. Trop J Pharm Res. 2008;seven:1089–99. [Google Scholar]

86. Vidya Advert, Devasagayam TP. Current status of Herbal drug in Republic of india: An overview. J Clin Biochem Nutr. 2007;41:1–11. [PMC complimentary article] [PubMed] [Google Scholar]

Articles from Pharmacognosy Reviews are provided here courtesy of Wolters Kluwer -- Medknow Publications

lynchrommed.blogspot.com

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249911/