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

  • Journal List
  • Pharmacogn Rev
  • v.four(8); Jul-December 2010
  • PMC3249911

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

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

Five. Lobo

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

A. Patil

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

A. Phatak

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

Northward. Chandra

Department of Botany, Birla Higher, Kalyan – 421 304, Maharastra, India.

Received 2010 Mar 4; Revised 2010 Mar eight

Abstract

In recent years, there has been a swell bargain of attending toward the field of free radical chemistry. Gratis radicals reactive oxygen species and reactive nitrogen species are generated past our trunk past various endogenous systems, exposure to unlike physiochemical conditions or pathological states. A remainder between complimentary radicals and antioxidants is necessary for proper physiological function. If gratis radicals overwhelm the torso'due south ability to regulate them, a condition known as oxidative stress ensues. Costless radicals thus adversely modify lipids, proteins, and Dna and trigger a number of human diseases. Hence awarding of external source of antioxidants can help in coping this oxidative stress. Synthetic antioxidants such as butylated hydroxytoluene and butylated hydroxyanisole have recently been reported to be unsafe for man health. Thus, the search for effective, nontoxic natural compounds with antioxidative activity has been intensified in recent years. The present review provides a brief overview on oxidative stress mediated cellular damages and role of dietary antioxidants every bit 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 biological science is producing a medical revolution that promises a new age of wellness and illness direction.[1] It is ironic that oxygen, an element indispensable for life,[2] under certain situations has deleterious effects on the human body.[3] Most of the potentially harmful furnishings of oxygen are due to the formation and action of a number of chemical compounds, known equally ROS, which have a tendency to donate oxygen to other substances. Free radicals and antioxidants have become commonly used terms in mod discussions of disease mechanisms.[iv]

Gratuitous RADICALS

A free radical can be defined as whatsoever molecular species capable of independent existence that contains an unpaired electron in an diminutive orbital. The presence of an unpaired electron results in sure mutual backdrop that are shared by most radicals. Many radicals are unstable and highly reactive. They tin 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 free radicals in many affliction 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 as Deoxyribonucleic acid, proteins, carbohydrates, and lipids.[6] Gratis radicals attack important macromolecules leading to cell harm and homeostatic disruption. Targets of gratis radicals include all kinds of molecules in the body. Among them, lipids, nucleic acids, and proteins are the major targets.

Product of free radicals in the human being body

Costless radicals and other ROS are derived either from normal essential metabolic processes in the human body or from external sources such as exposure to X-rays, ozone, cigarette smoking, air pollutants, and industrial chemicals.[3] Gratuitous radical formation occurs continuously in the cells as a upshot of both enzymatic and nonenzymatic reactions. Enzymatic reactions, which serve as source of free radicals, include those involved in the respiratory chain, in phagocytosis, in prostaglandin synthesis, and in the cytochrome P-450 system.[7] Free radicals can also be formed in nonenzymatic reactions of oxygen with organic compounds every bit well every bit those initiated past 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 fume

  • Environmental pollutants

  • Radiation

  • Certain drugs, pesticides

  • Industrial solvents

  • Ozone

Complimentary radicals in biology

Gratuitous radical reactions are expected to produce progressive adverse changes that accumulate with age throughout the body [Table i]. Such "normal" changes with age are relatively common to all. Even so, superimposed on this common pattern are patterns influenced by genetics and environmental differences that modulate complimentary radical damage. These are manifested as diseases at certain ages determined by genetic and ecology factors. Cancer and atherosclerosis, ii major causes of expiry, are salient "free radical" diseases. Cancer initiation and promotion is associated with chromosomal defects and oncogene activation. It is possible that endogenous free radical reactions, similar those initiated by ionizing radiations, may consequence in tumor germination. The highly significant correlation between consumption of fats and oils and expiry rates from leukemia and cancerous neoplasia of the chest, ovaries, and rectum among persons over 55 years may be a reflection of greater lipid peroxidation.[9] Studies on atherosclerosis reveal the probability that the affliction may exist due to free 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

Complimentary radicals[11–thirteen]

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 describe the condition 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 gratuitous radical production and antioxidant defenses, is associated with impairment to a wide range of molecular species including lipids, proteins, and nucleic acids.[fifteen] 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 (e.g., xanthine oxidase, lipogenase, cyclooxygenase) activation of phagocytes, release of free iron, copper ions, or a disruption of the electron transport chains of oxidative phosphorylation, producing excess ROS. The initiation, promotion, and progression of cancer, also every bit the side-effects of radiation and chemotherapy, have been linked to the imbalance betwixt ROS and the antioxidant defence force arrangement. ROS have been implicated in the induction and complications of diabetes mellitus, age-related middle disease, and neurodegenerative diseases such as Parkinson'south disease.[16]

Oxidative stress and human being diseases

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

Cardiovascular diseases

Heart diseases continue to be the biggest killer, responsible for virtually half of all the deaths. The oxidative events may affect cardiovascular diseases therefore; information technology has potential to provide enormous benefits to the health and lifespan. Poly unsaturated fatty acids occur as a major role of the low density lipoproteins (LDL) in blood and oxidation of these lipid components in LDL play a vital role in atherosclerosis.[xviii] The 3 most important cell types in the vessel wall are endothelial cells; smooth muscle jail cell and macrophage can release free radical, which affect lipid peroxidation.[19] With continued loftier level of oxidized lipids, blood vessel impairment to the reaction process continues and tin lead to generation of foam cells and plaque the symptoms of atherosclerosis. Oxidized LDL is antherogenic and is thought to exist important in the formation of anthersclerosis plaques. Furthermore, oxidized LDL is cytotoxic and tin can straight harm endothelial cells. Antioxidants like B-carotene or vitamin Due east play a vital role in the prevention of diverse cardiovascular diseases.

Carcinogenesis

Reactive oxygen and nitrogen species, such as super oxide anion, hydrogen peroxide, hydroxyl radical, and nitric oxide and their biological metabolites likewise play an of import role in carcinogenesis. ROS induce DNA harm, as the reaction of gratis radicals with Dna includes strand break base modification and DNA protein cross-links. Numerous investigators have proposed participation of free radicals in carcinogenesis, mutation, and transformation; it is clear that their presence in biosystem could lead to mutation, transformation, and ultimately cancer. Induction of mutagenesis, the best known of the biological effect of radiation, occurs mainly through damage of DNA past the HO. Radical and other species are produced by the radiolysis, and besides by directly radiations effect on DNA, the reaction effects on DNA. The reaction of HO. Radicals is mainly improver to double bond of pyrimidine bases and brainchild of hydrogen from the carbohydrate 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 jail cell proliferation secondary to the protein phosphorylation. B-carotene may exist protective against cancer through its antioxidant office, because oxidative products can cause genetic damage. Thus, the photo protective properties of B-carotene may protect against ultraviolet calorie-free induced carcinogenesis. Immunoenhancement of B-carotene may contribute to cancer protection. B-carotene may also have anticarcinogenic effect past altering the liver metabolism effects of carcinogens.[20] Vitamin C may be helpful in preventing cancer.[21] The possible mechanisms by which vitamin C may affect carcinogenesis include antioxidant furnishings, blocking of germination of nitrosanimes, enhancement of the allowed response, and acceleration of detoxification of liver enzymes. Vitamin E, an important antioxidant, plays a role in immunocompetence past increasing humoral antibody protection, resistance to bacterial infections, prison cell-mediated immunity, the T-lymphocytes tumor necrosis cistron production, inhibition of mutagen formation, repair of membranes in Deoxyribonucleic acid, and blocking micro cell line formation.[22] Hence vitamin E may be useful in cancer prevention and inhibit carcinogenesis by the stimulation of the immune organization. The administration of a mixture of the higher up three antioxidant reveled the highest reduction in take chances of developing cardiac cancer.

Gratuitous radical and aging

The human body is in constant boxing to keep from aging. Research suggests that free radical damage to cells leads to the pathological changes associated with aging.[23] An increasing number of diseases or disorders, likewise as aging procedure itself, demonstrate link either straight or indirectly to these reactive and potentially destructive molecules.[24] The major mechanism of crumbling attributes to Dna or the accumulation of cellular and functional damage.[25] Reduction of free radicals or decreasing their charge per unit of production may delay aging. Some of the nutritional antioxidants will retard the crumbling process and forestall illness. Based on these studies, it appears that increased oxidative stress commonly occurs during the aging process, and antioxidant condition may significantly influence the furnishings of oxidative damage associated with advancing historic period. Research suggests that free radicals have a significant influence on crumbling, that complimentary radical harm can be controlled with adequate antioxidant defense, 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 poly peptide and DNA

Oxidative impairment to protein

Proteins can exist oxidatively modified in iii ways: oxidative modification of specific amino acid, gratis radical mediated peptide cleavage, and formation of protein cross-linkage due to reaction with lipid peroxidation products. Protein containing amino acids such as methionine, cystein, arginine, and histidine seem to be the most vulnerable to oxidation.[26] Free radical mediated protein modification increases susceptibility to enzyme proteolysis. Oxidative damage to protein products may affect the activity of enzymes, receptors, and membrane send. Oxidatively damaged poly peptide products may contain very reactive groups that may contribute to damage to membrane and many cellular functions. Peroxyl radical is usually considered to be free radical species for the oxidation of proteins. ROS tin can damage proteins and produce carbonyls and other amino acids modification including formation of methionine sulfoxide and poly peptide carbonyls and other amino acids modification including formation of methionine sulfoxide and protein peroxide. Poly peptide oxidation affects the amending of signal transduction machinery, enzyme activity, 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 equally aging, artheroscleosis, inflammation and carcinogenesis, and drug toxicity. Lipid peroxidation is a free radical process involving a source of secondary costless radical, which further can human activity as second messenger or can directly react with other biomolecule, enhancing biochemical lesions. Lipid peroxidation occurs on polysaturated fatty acrid located on the jail cell membranes and information technology further proceeds with radical chain reaction. Hydroxyl radical is idea to initiate ROS and remove hydrogen cantlet, thus producing lipid radical and further converted into diene conjugate. Further, past addition of oxygen it forms peroxyl radical; this highly reactive radical attacks some other 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 example, alkanes, malanoaldehyde, and isoprotanes. These compounds are used as markers in lipid peroxidation assay and have 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 damage. Information technology has been reported that specially in aging and cancer, DNA is considered as a major target.[28] Oxidative nucleotide every bit glycol, dTG, and 8-hydroxy-2-deoxyguanosine is found to exist increased during oxidative harm to DNA nether UV radiations or free radical impairment. Information technology has been reported that mitochondrial Deoxyribonucleic acid are more susceptible to oxidative damage that have role in many diseases including cancer. It has been suggested that 8-hydroxy-two-deoxyguanosine can be used every bit biological marking for oxidative stress.[29]

ANTIOXIDANTS

An antioxidant is a molecule stable enough to donate an electron to a rampaging gratis radical and neutralize it, thus reducing its capacity to damage. These antioxidants delay or inhibit cellular impairment mainly through their gratis radical scavenging holding.[30] These low-molecular-weight antioxidants can 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 trunk.[31] Other lighter antioxidants are institute in the diet. Although there are several enzymes system within the body that scavenge free radicals, the principle micronutrient (vitamins) antioxidants are vitamin Eastward (α-tocopherol), vitamin C (ascorbic acid), and B-carotene.[32] The torso cannot manufacture these micronutrients, then they must exist 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 study was devoted to the uses of antioxidants in important industrial processes, such as the prevention of metal corrosion, the vulcanization of safe, and the polymerization of fuels in the fouling of internal combustion engines.[33]

Early enquiry on the office of antioxidants in biological science focused on their use in preventing the oxidation of unsaturated fats, which is the crusade of rancidity.[34] Antioxidant activity could exist measured simply by placing the fat in a closed container with oxygen and measuring the rate of oxygen consumption. Nevertheless, it was the identification of vitamins A, C, and E every bit 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 action of antioxidants were start explored when it was recognized that a substance with antioxidative activity is probable to be one that is itself readily oxidized.[37] Research into how vitamin E prevents the procedure of lipid peroxidation led to the identification of antioxidants as reducing agents that forbid oxidative reactions, often by scavenging ROS earlier they can damage cells.[38]

Antioxidant defense system

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 exist in the intracellular and extracellular environment to detoxify ROS.[39]

Mechanism of action of antioxidants

Two principle mechanisms of action have been proposed for antioxidants.[40] The first is a chain- breaking mechanism by which the primary antioxidant donates an electron to the complimentary radical present in the systems. The second mechanism involves removal of ROS/reactive nitrogen species initiators (secondary antioxidants) by quenching chain-initiating goad. Antioxidants may exert their effect on biological systems by unlike mechanisms including electron donation, metal ion chelation, co-antioxidants, or by gene expression regulation.[41]

Levels of antioxidant action

The antioxidants acting in the defense systems act at unlike levels such as preventive, radical scavenging, repair and de novo, and the fourth line of defense, i.e., the adaptation.

The kickoff line of defense is the preventive antioxidants, which suppress the formation of gratis 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 water, 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 corresponding alcohols. PHGPX is unique in that it can reduce hydroperoxides of phospholipids integrated into biomembranes. Glutathione peroxidase and catalase reduce hydrogen peroxide to h2o.

The 2nd line of defense is the antioxidants that scavenge the active radicals to suppress concatenation 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 Eastward and ubiquinol are lipophilic radical-scavenging antioxidants. Vitamin E is accepted as the nearly 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 forestall the accumulation of oxidized proteins.

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

There is another important office called adaptation where the point for the product and reactions of free radicals induces formation and transport of the appropriate antioxidant to the right site.[42]

ENZYMATIC

Types of antioxidants

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

Superoxide dismutase

Superoxide dismutases (SODs) are a class of closely related enzymes that catalyze the breakdown of the superoxide anion into oxygen and hydrogen peroxide.[45,46] SOD enzymes are nowadays in about all aerobic cells and in extracellular fluids.[47] There 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 atomic number 26 or manganese), and finally the Ni type which binds nickel.[48] In higher plants, SOD isozymes have been localized in different jail cell compartments. Mn-SOD is nowadays in mitochondria and peroxisomes. Atomic number 26-SOD has been found 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 (as in all other mammals and most chordates), three forms of superoxide dismutase are present. SOD1 is located in the cytoplasm, SOD2 in the mitochondria, and SOD3 is extracellular. The first is a dimer (consists of ii units), while the others are tetramers (four subunits). SOD1 and SOD3 contain copper and zinc, while SOD2 has manganese in its reactive center.[51]

Catalase

Catalase is a mutual enzyme found in nearly 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 prevent impairment, it must be quickly converted into other, less dangerous substances. To this end, catalase is often used by cells to apace catalyze the decomposition of hydrogen peroxide into less reactive gaseous oxygen and h2o molecules.[53] All known animals use catalase in every organ, with specially high concentrations occurring in the liver.[54]

Glutathione systems

The glutathione system includes glutathione, glutathione reductase, glutathione peroxidases, and glutathione S-transferases. This system is establish in animals, plants, and microorganisms.[55] Glutathione peroxidase is an enzyme containing four selenium-cofactors that catalyze the breakdown of hydrogen peroxide and organic hydroperoxides. In that location are at least four dissimilar glutathione peroxidase isozymes in animals.[56] Glutathione peroxidase 1 is the most abundant and is a very efficient scavenger of hydrogen peroxide, while glutathione peroxidase 4 is most active with lipid hydroperoxides. The glutathione Southward-transferases prove high activity with lipid peroxides. These enzymes are at specially high levels in the liver and as well 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] About other animals are able to produce this compound in their bodies and do not require it in their diets. In cells, it is maintained in its reduced form by reaction with glutathione, which can be catalyzed by protein disulfide isomerase and glutaredoxins.[59] Ascorbic acid is a reducing agent and tin can reduce and thereby neutralize ROS such equally hydrogen peroxide.[60] In improver to its direct antioxidant effects, ascorbic acid is also a substrate for the antioxidant enzyme ascorbate peroxidase, a function that is specially important in stress resistance in plants.[61]

Glutathione

Glutathione is a cysteine-containing peptide establish in mostforms of aerobic life.[62] It is not required in the diet and is instead synthesized in cells from its constituent amino acids. Glutathione has antioxidant properties since the thiol grouping in its cysteine moiety is a reducing agent and can exist reversibly oxidized and reduced. In cells, glutathione is maintained in the reduced course by the enzyme glutathione reductase and in turn reduces other metabolites and enzyme systems as well as reacting directly with oxidants.[63] Due to its high concentration and key role in maintaining the cell'southward redox land, glutathione is 1 of the most important cellular antioxidants.[33] In some organisms, glutathione is replaced by other thiols, such as past mycothiol in the actinomycetes, or by trypanothione in the kinetoplastids.[64]

Melatonin

Melatonin, also known chemically as North-acetyl-v-methoxytryptamine,[65] is a naturally occurring hormone found in animals and in some other living organisms, including algae.[66] Melatonin is a powerful antioxidant that tin easily cantankerous cell membranes and the claret–brain barrier.[67] Unlike other antioxidants, melatonin does not undergo redox cycling, which is the power of a molecule to undergo repeated reduction and oxidation. Melatonin, in one case oxidized, cannot be reduced to its former state because information technology forms several stable end-products upon reacting with costless radicals. Therefore, it has been referred to every bit a final (or suicidal) antioxidant.[68]

Tocopherols and tocotrienols (Vitamin Due east)

Vitamin E is the collective proper noun for a prepare of eight related tocopherols and tocotrienols, which are fat-soluble vitamins with antioxidant backdrop.[69] Of these, α-tocopherol has been near studied every bit it has the highest bioavailability, with the body preferentially absorbing and metabolizing this class.[70] It has been claimed that the α-tocopherol form is the near important lipid-soluble antioxidant, and that it protects membranes from oxidation by reacting with lipid radicals produced in the lipid peroxidation concatenation reaction.[71] This removes the gratis radical intermediates and prevents the propagation reaction from continuing. This reaction produces oxidized α-tocopheroxyl radicals that tin be recycled back to the active reduced grade through reduction by other antioxidants, such every bit ascorbate, retinol, or ubiquinol.[72]

Uric acid

Uric acid accounts for roughly one-half the antioxidant power of plasma. In fact, uric acrid may take substituted for ascorbate in human development.[73] However, like ascorbate, uric acid tin can also mediate the product of active oxygen species.

PLANTS AS SOURCE OF ANTIOXIDANTS

Synthetic and natural nutrient antioxidants are used routinely in foods and medicine especially those containing oils and fats to protect the food confronting oxidation. There are a number of synthetic phenolic antioxidants, butylated hydroxytoluene (BHT) and butylated hydroxyanisole (BHA) being prominent examples. These compounds have been widely uses every bit antioxidants in food industry, cosmetics, and therapeutic industry. However, some physical properties of BHT and BHA such as their loftier volatility and instability at elevated temperature, strict legislation on the use of constructed food additives, carcinogenic nature of some constructed antioxidants, and consumer preferences have shifted the attention of manufacturers from synthetic to natural antioxidants.[74] In view of increasing risk factors of human to diverse deadly diseases, in that location has been a global trend toward the use of natural substance nowadays in medicinal plants and dietary plats equally therapeutic antioxidants. Information technology has been reported that there is an inverse relationship between the dietary intake of antioxidant-rich food and medicinal plants and incidence of human diseases. The use of natural antioxidants in food, corrective, and therapeutic manufacture would be promising alternative for constructed antioxidants in respect of depression cost, highly compatible with dietary intake and no harmful effects inside the human torso. Many antioxidant compounds, naturally occurring in found sources accept been identified as complimentary radical or active oxygen scavengers.[75] Attempts have been made to report the antioxidant potential of a wide variety of vegetables like potato, spinach, tomatoes, and legumes.[76] At that place are several reports showing antioxidant potential of fruits.[77] Potent antioxidants activities have been found in berries, cherries, citrus, prunes, and olives. Light-green and blackness teas have been extensively studied in the recent past for antioxidant properties since they contain upwards to 30% of the dry weight as phenolic compounds.[78]

Apart from the dietary sources, Indian medicinal plants also provide antioxidants and these include (with mutual/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 leaf), 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 (Center leaved moonseed, Guduchi), Trigonella foenum-graecium (Fenugreek), Withania somifera (Wintertime reddish, Ashwangandha), and Zingiber officinalis (Ginger).[79]

ANTIOXIDANT POTENTIAL OF INDIAN FUNCTIONAL FOODS

Concepts of functional foods and nutraceuticals

In the terminal decade, preventive medicine has undergone a swell accelerate, peculiarly in developed countries. Enquiry has demonstrated that nutrition plays a crucial role in the prevention of chronic diseases, equally most of them can be related to diet. Functional nutrient enters the concept of considering nutrient not merely necessary for living simply likewise as a source of mental and physical well-being, contributing to the prevention and reduction of risk factors for several diseases or enhancing certain physiological functions.[fourscore] A nutrient can be regarded as functional if information technology is satisfactorily demonstrated to affect beneficially one or more target functions in the body, across acceptable nutritional effects, in a way which is relevant to either the state of well being and health or reduction of the adventure of a disease. The benign furnishings could exist either maintenance or promotion of a land of well being or health and/or a reduction of take a chance of a pathologic process or a disease.[81] Whole foods stand for the simplest example of functional nutrient. Broccoli, carrots, and tomatoes are considered functional foods because of their loftier contents of physiologically active components (sulforaphen, B-carotene, and lycopene, respectively). Greenish vegetables and spices like mustard and turmeric, used extensively in Indian cuisine, also tin autumn under this category.[82] "Nutraceutical" is a term coined in 1979 by Stephen DeFelice.[83] It is defined "as a nutrient or parts of food that provide medical or health benefits, including the prevention and treatment of illness." 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 any nontoxic food extract supplement that has scientifically proven health benefits for both the treatment and prevention of disease.[84] The increasing involvement in nutraceuticals reflects the fact that consumers hear nearly epidemiological studies indicating that a specific diet or component of the diet is associated with a lower hazard for a sure disease. The major active nutraceutical ingredients in plants are flavonoids. As is typical for phenolic compounds, they can act equally potent antioxidants and metal chelators. They also have long been recognized to possess anti-inflammatory, antiallergic, hepatoprotective, antithrombotic, antiviral, and anticarcinogenic activities.[85]

Indian dietary and medicinal plants as functional foods

Ingredients that make food functional are dietary fibers, vitamins, minerals, antioxidants, oligosaccharides, essential fatty acids (omega-3), lactic acrid bacteria cultures, and lignins. Many of these are nowadays in medicinal plants. Indian systems of medicine believe that complex diseases can exist treated with circuitous combination of botanicals unlike in due west, with single drugs. Whole foods are hence used in India every bit functional foods rather than supplements. Some medicinal plants and dietary constituents having functional attributes are spices such every bit onion, garlic, mustard, red chilies, turmeric, clove, cinnamon, saffron, curry leaf, fenugreek, and ginger. Some herbs as Bixa orellana and vegetables similar 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]

Determination

Free radicals damage contributes to the etiology of many chronic health problems such equally cardiovascular and inflammatory disease, cataract, and cancer. Antioxidants forestall gratuitous radical induced tissue damage by preventing the formation of radicals, scavenging them, or by promoting their decomposition. Constructed antioxidants are recently reported to exist dangerous to human health. Thus the search for effective, nontoxic natural compounds with antioxidative activity has been intensified in contempo years. In add-on to endogenous antioxidant defense systems, consumption of dietary and plant-derived antioxidants appears to be a suitable alternative. Dietary and other components of plants class a major source of antioxidants. The traditional Indian diet, 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 ane strategy that is gaining importance.

Newer approaches utilizing collaborative inquiry and modern engineering science in combination with established traditional health principles volition yield dividends in virtually future in improving health, particularly amongst people who do non accept access to the apply of costlier western systems of medicine.

Footnotes

Source of Back up: Nada

Conflict of Involvement: None declared

REFERENCES

i. 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 defense mechanism. Saudi Pharm J. 2004;12:1–18. [Google Scholar]

3. Bagchi K, Puri Southward. Free radicals and antioxidants in health and disease. East Mediterranean Health Jr. 1998;4:350–threescore. [Google Scholar]

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

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

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

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

9. Lea AJ. Dietary factors associated with death rates from sure neoplasms in man. Lancet. 1966;2:332–iii. [PubMed] [Google Scholar]

10. Harman D. Role of gratis radicals in aging 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 Biology of Parasites. London: Academic Press; 1995. pp. 147–60. [Google Scholar]

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

fourteen. Stone 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 costless radicals and oxidative stress. Am J Med. 2000;108:652–9. [PubMed] [Google Scholar]

16. Rao AL, Bharani M, Pallavi V. Function of antioxidants and free radicals in wellness and disease. Adv Pharmacol Toxicol. 2006;7:29–38. [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. Consequence of antioxidants on oxidative modification of LDL. Ann Med. 1991;23:573–81. [PubMed] [Google Scholar]

xix. Neuzil J, Thomas SR, Stocker R. Requirement for promotion, or inhibition of α- tocopherol of radical induced initiation of plasma lipoprotein lipid peroxidation. Complimentary 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 BE, Horing DH, Moser U. The function 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 aging. Exp Gerontol. 1999;34:293–303. [PubMed] [Google Scholar]

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

25. Cantuti-Castelvetri I, Shukitt-Hale B, Joseph JA. Neurobehavioral aspects of antioxidants in crumbling. Int J Dev Neurosci. 2000;18:367–81. [PubMed] [Google Scholar]

26. Freeman BA, Crapo JD. Biology of illness: 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 acid 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 harm. Nature. 1998;394:700–iv. [PubMed] [Google Scholar]

29. Hattori Y, Nishigori C, Tanaka T, Ushida Thousand, Nikaido O, Osawa T. eight Hydroxy-ii-deoxyguanosine is increased in epidermal cells of hairless mice after chronic ultraviolet B exposure. J Invest Dermatol. 1997;89:10405–9. [PubMed] [Google Scholar]

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

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

32. Levine G, 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;xvi:177–92. [PubMed] [Google Scholar]

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

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

36. Knight J. Gratuitous radicals: Their history and current status in aging and affliction. 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;135:363–6. [PubMed] [Google Scholar]

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

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

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

42. Niki E. Antioxidant defenses in eukaryotic cells. In: Poli G, Albano East, 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 Wellness Perspect. 1998;106:1219–28. [PMC free article] [PubMed] [Google Scholar]

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

46. Banniste J, Bannister W, Rotilio Chiliad. Aspects of the construction, 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 touch on 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 K. Crystal structure of nickel-containing superoxide dismutase reveals some other type of agile site. Proc Natl Acad Sci. 2004;101:8569–74. [PMC complimentary 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 establish cells. Trends Plant Sci. 2001;6:145–50. [PubMed] [Google Scholar]

50. Corpas FJ, Fernández-Ocaña A, Carreras A, Valderrama R, Luque F, Esteban FJ, et al. The expression of unlike superoxide dismutase forms is jail cell-type dependent in olive (Olea europaea 50.) leaves. Plant Jail 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 commodity] [PubMed] [Google Scholar]

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

53. Gaetani G, Ferraris A, Rolfo M, Mangerini R, Arena S, Kirkman H. Predominant part of catalase in the disposal of hydrogen peroxide within homo erythrocytes. Blood. 1996;87:1595–9. [PubMed] [Google Scholar]

54. Eisner T, Aneshansley DJ. Spray aiming in the bombardier beetle: Photographic testify. Proc Natl Acad Sci United states. 1999;96:9705–9. [PMC gratis commodity] [PubMed] [Google Scholar]

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

56. Brigelius-Flohe R. Tissue-specific functions of individual glutathione peroxidases. Gratis 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. Fifty-ascorbicacid biosynthesis. Vitam Horm. 2001;61:241–66. [PubMed] [Google Scholar]

59. Meister A. Glutathione-ascorbic acrid 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 as an antioxidant: Evaluation of its role in disease prevention. J Am Coll Nutr. 2003;22:eighteen–35. [PubMed] [Google Scholar]

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

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

63. Meister A. Glutathione metabolism and its selective modification. J Biol Chem. 1988;263:17205–8. [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 E, Mulligan C, Taylor Fifty, Kerksick C, Galbreath Thou, Greenwood M, et al. Effects of a single dose of Northward-Acetyl-v-methoxytryptamine (Melatonin) and resistance exercise on the growth hormone/IGF-1 axis in young males and females. J Int Soc Sports Nutr. 2007;four:xiv. [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–vii. [PubMed] [Google Scholar]

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

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

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

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

71. Traber MG, Atkinson J. Vitamin East, antioxidant and goose egg more. Free Radic Biol Med. 2007;43:4–15. [PMC free article] [PubMed] [Google Scholar]

72. Wang Ten, Quinn P. Vitamin Due 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. Diet and antioxidant status. Food Chem Toxicol. 1999;37:999–1007. [PubMed] [Google Scholar]

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

76. Furuta Due south, Nishiba Y, Suda I. Fluorometric analysis for screening antioxidative activities of vegetables. J Nutrient 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 black teas. J Agric Food Chem. 1998;46:3635–42. [Google Scholar]

79. Devasagayam TP, Tilak JC, Boloor KK, Sane KS, Ghaskadbi SS, Lele RD. Costless radicals and antioxidants in Human Wellness: Current status and future prospects. J Assoc Physicians India. 2004;52:794–803. [PubMed] [Google Scholar]

80. López-Varela S, González-Gross One thousand, 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 health? The concept of functional food. Food Chem Toxicol. 1999;37:1034–41. [PubMed] [Google Scholar]

82. Krishnaswamy M. Indian functional nutrient: Function in prevention of cancer. Nutr Rev. 1996;54:127–31. [PubMed] [Google Scholar]

83. DeFelice SL. Nutraceuticals: Opportunities in an Emerging Market. Scrip Mag. 1992;9:14–v. [Google Scholar]

84. Dillard CJ, German JB. Phytochemicals: Nutraceuticals and human being wellness. J Sci Food Agric. 2000;80:1744–56. [Google Scholar]

85. Tapas AR, Sakarkar DM, Kakde RB. Review article flavonoids as nutraceuticals: A review. Trop J Pharm Res. 2008;7:1089–99. [Google Scholar]

86. Vidya AD, Devasagayam TP. Current status of Herbal drug in India: An overview. J Clin Biochem Nutr. 2007;41:i–11. [PMC free article] [PubMed] [Google Scholar]


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


petersontial1966.blogspot.com

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

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

Postar um comentário

Iklan Atas Artikel

Iklan Tengah Artikel 1

Iklan Tengah Artikel 2

Iklan Bawah Artikel