Classification According To Maturity Biology Essay

categorization According To Maturity Biology EssayINTRODUCTIONThe gracious nerve center is very nearly spherical, with a diameter of approximately 24 mm (nearly one inch). It consists of three concentric layers, each with its own peculiarity appearance, structure and functions. From outer nearly to innermost, the three layers be the sclera, which protects the mallball the choroid, which nourishes the eyeball and the retina, which detects clean-living and initiates neural messages bound for the humour. The eye is partitioned into both chambers, a small anterior chamber and a larger vitreous chamber. gum olibanum the staple fiber layout consists of three concentric layers, two chambers, iris, pupil and the lense of the eye (Ross and wilson, 2001).Fig.1 Anatomy of the eyeCUsersDHINESHDesktopUntitled1.pngThe Lens maven of very important optical element of the eye, the crystalline lens, lies right behind the iris. The lens takes its name from its proportion to a lentil, or b ean. In adults, the lens is shaped or so 9 mm in diameter and 4 mm in thickness. The lens consists of three distinct parts an elastic coering, or contr body process an epithelial layer just inside the ejector seat and the lens itself.The thin, elastic condensing around the lens has two jobs. First, it moderates the flow of aqueous humor into the lens, helping the lens retain its transp bency to light. Second, the elastic wrap moulds the shape of the lens varying its flatness and, thitherby, the lens optical federal agency. This variant in optical power is called accommodation.Lens grows throughout the life span the outer, epithelial layer of lens continues to produce protein fibres that argon added to the advance of the lens. Consequently, those protein fibres nearest the heart and soul of the lens are the oldest (some were present at birth), whereas the fibres on the outside are the youngest. amongst birth and 90 years of age, the lens quadruples in thickness and attains a weight of 250 mg. In the centre of the lens, the old fibres become more densely packed, producing sclerosis, or hardening, of the lens (Paterson, 1979).For good vision, the lens must be transparent and light must be able to pass through it easily, without loss or deviation. kindred the cornea, this transparency depends on the material out of which the lens is made. Of all the bodys parts, the lens has the highest percentage of protein, and its protein fibres are seamed up parallel to one an early(a), maximizing the lens transparency to light. Anything that disturbs this alignment such as extra fluid inside the lens reduces its transparency. An opacity (or reduced transparency) of the lens is called a cataract. While some cataracts are minor, barely reducing the transmission of light, others undermine vision to the extent of blindness (Kyselova, 2004).CataractCataract is the opacification and crystalline doation of eye lens, associated with the breakdown of the eye lens micro- architecture, which interferes with the transmission of light onto the retina. Several biochemical carry outes for example, calcium deposition, aerobic stress, variant transition, altered epithelial metabolism, crystalline precipitation, calpain- scram proteolysis and cytoskeletal loss takes place during the instruction of cataract (Moghaddam, 2005).Fig.2 Normal, clear lens Fig.3 Lens foggy by cataractCUsersDHINESHDesktopUntitled.pngFig.4 Etiology of cataract (Jacob, 1999)CUsersDHINESHDesktopUntitled.pngTYPES OF CATARACTA. Acquired cataract1. Age related cataracta) Morphological classificationi) Subcapsular cataractAnterior subcapsular cataract in general associated with fibrous metaplasia of the epithelium present below the lens capsule. rear subcapsular cataract lies just in front of the shag capsule and a clear vacuolated, granular or plaque-like appearance. Near vision is also most oft impaired more than distant vision.ii) Nuclear cataract usually begins as an amplificat ion of the changes most ofttimes seen with linguistic rule aging lens nucleus. It is often related with change magnitude spherical aberration and also with an increased deflective index leading to myopia. Some elderly patients whitethorn consequently be capable to read tho again without spectacles.iii) Cortical cataract may be associated with the anterior, posterior or equatorial cortex. The opacities begin as clefts and vacuoles amidst lens fibres be begin of hydration of the cortex. both(prenominal) cortical and subcapsular cataracts are white on oblique illumination and show shocking colouration, silhouetted against the red reflex, on retroillumination.b) Classification according to maturityi) An immature cataract means partially opaque lens.ii) A mature cataract means completely opaque lens.iii) A hypermature cataract means the leakage of water from the lens it leads to wrinkly and shrunken anterior capsule.iv) A morgagnian cataract means the total liquefication of lens cortex like hypermature cataract and it allows the lens nucleus to shrink inferiorly (Hejtmancik, 2004).2. Presenile cataractCataract may develop early in the following conditions,a) Diabetes mellitusTypically diabetic cataract is rare. In hyperglycemic conditions, the aqueous humor secretes high direct of glucose and this excess of glucose diffuses into the lens. Aldosereductase metabolises glucose to sorbitol, which then accumulates in the lens, closureing in secondary osmotic over hydration of the lens substance. Nuclear opacities are common and tend to grow rapidly. Premature dystrophy may be seen due to decreased pliability of the lens.b) Myotonic dystrophyAbout 90% of patients, in third ten-spot convey fine cortical iridescent opacities, which evolve into visually disabling stellate posterior subcapsular cataract by the fifth decade.c) Atopic dertmatitisAbout 10% of patients with severe atopic dermatitis develop cataracts in the second to fourth decades. The opacities ar e often bilateral and may mature quickly. Shield like anterior subcapsular plaque which wrinkles the anterior capsule is characteristic. Posterior subcapsular opacities resembling a complicated cataract may also occur.3. Traumatic cataractTrauma is the major risk factor for coloured cataract in individuals. The following risk factors are involved in traumatic cataract,a) Direct penetrating brand to the lens.b) Concussion may cause an imprinting of iris colour on the anterior lens capsule (Vossius ring) as flower shaped cortical opacities (rosette cataract).c) Electric shock and lightening are rare causes.d) Ionizing radiation.e) invisible radiation- In glassblowers, the IR rays causes exfoliation of the lens capsule which expirations in thickening of the superficial portion of the capsule and it further splits the deeper layer and protrudes into the anterior chamber.B. Drug induced cataracta) Steroidal drugs may induce cataract. Initially the lens opacities organize in posteri or subcapsular region spreads into the anterior region. The relation between dose, duration of administration and the cataract development is unclear. It is understood that children may be more at risk to the cataractogenic cases of systemic steroids and genetic talent may also be of significance. Patients who develop lens physiologic changes should have their dose decreased to a minimum, reliable with control of the underlying disease, and if feasible be considered for alternate drug therapy. Premature opacities may lapsing if therapy is discontinued, alternatively progression may occur despite withdrawn and warrant surgical intervention.b) Chlorpromazine may cause the deposit of innocuous fine, stellate, yellowish brown granules on the anterior lens capsule inwardly the papillary area. The deposition of granular material may accumulate on the corneal endothelium and deep stroma. Both lenticular and corneal deposits are dose -related and irreversible. In very high doses (2400 mg daily), this drug may cause retinotoxicity.c) Lens opacities may occur due to the irregular use of Busulphan (Myleran) for the treatment of chronic myeloid leukaemia.d) Amiodarone, utilise in the treatment of cardiac arrhythmias, causes visually inconsequential anterior subcapsular lens deposits in about 50% of patients on moderate to high doses.e) Gold used in the treatment of rheumatoid arthritis, causes stainless anterior capsular deposits in about 50% of patients on treatment for more than 3 years.f) Allopurinol, used in the treatment of hyperuricaemia and chronic gout, increases the risk of cataract establishation in elderly patients, if the cumulative does exceeds 400 g or duration of administration exceeds 3 years.C. Secondary cataractA secondary (complicated) cataract grows as a result of some other primary ocular diseases.i. Chronic anterior uveitis is the main cause of secondary cataract. The earliest finding is a polychromatic lustre at the posterior pole of the l ens which may not progress if the uveitis is arrested. If the inflammation persists, posterior and anterior opacities developed may progress to maturity.ii. Acute congestive tap closure glaucoma may cause small grey white anterior, subcapsular or capsular opacities at bottom the papillary area.a. Myopia (Pathological) is linked with posterior subcapsular lens opacities and early-onset nuclear sclerosis, which may ironically increase the myopic refractile error. Simple myopia, however, is not associated with such cataract abidanceation.b. Hereditary dystrophies such as retinitis pigmentosa, gyrate atrophy, leper congenital amaurosis and stickler syndrome may be associated with posterior subcapsular lens opacities. Cataract surgery may occasionally improve visual acuity even in the presence of severe retinal changes (Kanski et al., 2003). exonerate radicals involved in cataractogenesisFree radicals may be formed either by the reduction of tittles by electron transfer or by the hae molytic partition of covalent bond. Both these reactions may be enzymatic or non-enzymatic.Due to the presence of an odd leftover electron in its outermost orbital, these sluttish radicals are unstable and readily react with neighbourhood molecules and natural selection electrons from them, converting the attacked molecule into a few radical, which in bust attacks another molecule generating more free radicals and so on. This enables free radicals to induce drawing string reactions that may be thousands of events long. A free radical reaction is alter by reaction between two free radicals or neutralization by antioxidants (Uday et al., 1999).Fig.5 Pathways of ROS formationCUsersDHINESHDesktopUntitled 3.pngGeneration of free radicalsBiological free radicals include labile oxygen species, reactive nitrogen species, reactive sulphur species, free radicals obtained form xenobiotics.a) Su bleach anion radical (O2.-)It is drived from nicotinamide adenine dinucleotide phosphateH o xidase and from mitochondria.i) NADPH oxidase is present in the lysosomal cell membranes. It steals electron from O2 resulting in the formation su bleach anion radical (O2-). It is converted to hydrogen peroxide and is a spontaneous reaction which is know as respiratory burst. This hydrogen peroxide may react with the chlorine in the presence of myeloperoxidase to form hypochlorous acid or it may produce hydroxyl radicals, by the Fenton reaction which uses the metal ion Fe3+.ii) From Mitochondria Ubiquionone, which is a concluding acceptor of electron, is converted to semiquinone (free radical). By reacting with O2, it forms (O2-) super oxide radical with piddle2, it produce hydroxyl radical ion.b) atomic number 1 PeroxideH2O2sodomist It is formed by the dismutation of superoxide by the enzyme superoxide dismutase.O 2 + O2 Hydrogen peroxide is generated fromi) Aminoacid oxidases Flavin is a co-enzyme required for the oxidative deamination of amino acid. The reduced flavin attac ks molecular oxygen to form hydrogen peroxide.ii) Xanthine oxidase Xanthine oxidase catalyses the conversion of hypoxanthine to xanthine and hydrogen peroxide is released from molecular oxygen.iii) Peroxisomes Peroxisomes is the order of -oxidation of fatty acids. - Oxidation of the fatty acids is catalysed by acetyl co-enzyme-A dehydrogenase. During this process, a co-enzyme called FAD which donates two electrons gets reduced to FADH2. Again it is converted to FAD. During that process it gives out O2 and H2O (Kovaceva et al., 2007).c) Hydroperoxyl radicalThey are extremely lipophillic and capable of initiating lipid peroxidation.Lipid peroxidationLipid peroxidation is a self- perpetuating common process and involves the conversion of lipid components from cell organelles into lipid peroxides resulting in the formation of a pigment known as lipofuscin. Lysosomic reactive oxygen species are formed as a result of complex oxidative chain reactions in mitochondria during energy produ ctionion. H2O2 formed in smaller amounts by mitochondria pass through walls of lysosome and react with Fe (II) in a reaction known as Fenton reaction to form potent hydroxyl radicals which cause lipid peroxidation (Halliwell, 2001). Malondialdehyde is the major reactive aldehyde resulting from the peroxidation of biological membrane polyunsaturated fatty acids (PUFA). MDA, a secondary product of LPO, is used as an indicator of tissue damage by a series of chain reactions. MDA is a by-product of prostaglandin biosynthesis. It reacts with thiobarbituric acid and produces a red-coloured product. MDA is a mutagenic and genotoxic agent that may contribute to development of piece cancer.Ca2+ ATPaseThe Ca2+ ATPase is a transport protein in the cells that serves to eliminate calcium (Ca2+) from the cell. It is essential for maintaining the amount of Ca2+ within the cells. Based upon the electrochemical gradient calcium ion enter into the cells through the trans membrane. This process is im portant for the cell signalling by which it lowers calcium level. Thus it is necessary for the cell to utilize ion pumps to remove the Ca2+. The Ca2+ ATPase is expressed in a variety of tissues, unneurotic with the brain (Hightower et al., 1982).IN VIVO MODELS IN CATARACT (Gupta, 2004)1. Sugar cataracti) Galactose induced cataractThe changes associated with galactose cataractogenesis include the initial reduction of galactose into dulcitol through intervention of aldose reductase with NADPH as a co-factor. Accumulation of dulcitol in the lens, (since it is not metabolized) creates cellular hypertonicity associated with and/or followed by a cascade of events, which includes an influx of water, swelling of the lens fibres, epithelial cell edema, damage of blood plasma membrane, compromise of cellular permeability, a drop in myinositol level, a reduction in Na+ K+ ATPase operation an influx of Na+ and Cl- and an efflux of K+ and the loss of glutathione and aminoacids. These are the morphological, biochemical, enzymatic and molecular alterations in the lens associated with galactose cataracts.ii) Alloxan induced cataractAlloxan is a cyclic urea analog which is highly reactive molecule that is readily reduced to dialuric acid, which is then auto oxidized back to alloxan resulting in the formation of hydroxyl radical, O2.-, including H2O2 (hydrogen peroxide). However, the other mechanism reveals the ability of alloxan to react with protein sulfhydryl groups on hexokinase, a signal recognition enzyme in the pancreatic -cells that couples changes in the blood glucose concentration to the rate of insulin secretion. By this mechanism, prohibition era of glucokinase and other SH containing membrane proteins on the -cells would eventually result in cell necrosis within minutes.iii) Streptozocin induced cataractDiabetes related cataractogenic changes are seen in the animals injected with streptozocin. This streptozocin initiates cytotoxic action in pancreatic cells because sreptozocin contain glucose molecule and highly reactive nitrosourea side chain. It binds to the membrane receptor to generate structural damage. At the intracellular level three major phenomena are responsible for cell death,i) Methylationii) Free radical productioniii) Formation of Nitric oxide (NO).The damage caused to cells alters the sugar metabolism leading to diabetes.2. Selenite induced cataractSelenite cataract resembles human cataract in many ways such as insoluble protein, vesicle formation, increased calcium, reduced glutathione (GSH) and decreased water-soluble proteins. However, selenite cataract shows no high molecular weight protein aggregation or increased disulfide formation and is predominate by rapid calpain-induced proteolytic precipitation, while senile cataracts may be produced by prolonged oxidative stress.3. Naphthalene induced cataractNaphthalene is oxidized in the liver initially to an epoxide and then it converted into naphthalene dihydrodio l. This stable component is converted enzymatically into dihydroxynaphthalene to stretchability the eye. Being unstable at physiologic pH, 1, 2- dihydroxynaphthalene and spontaneously autooxidises to 1, 2- naphthoquinone and H2O2 . It alkylates proteins, glutathione and aminoacids and generates free radicals.4. Glucocorticoid induced cataractGlucocorticoid cataract results in the formation of steroid- adduct protein, induction of transglutaminase and reduction of ATPase activity may lead to cataract. Steroid cataracts are produced by the activities of glucocorthicoids and progressed by way of production of oxidative stress similar to other types of cataract.5. L- Buthionine S, R- Sulfoximine (BSO) induced cataractGlutathione is present in mammalian lens in high concentrations and is involved in the protection of lens against oxidation. In most of the cataracts the decrease in its level is observed.6. Smoke induced cataractCigarette smoke contains trace and heavy metals. The inc reased metal contents in lens cause lens damage by the mechanism of oxidative stress-forming oxygen radicals, via metal catalyzed Fenton Reaction. In other words cigarette smoke is associated with the hookup of iron and calcium.7. UV radiation induced cataractEpidemiological studies have exposed a link between exposure to UV radiation in sunlight and development of cataract. Experimental studies confirm that ultraviolet (UV) radiation induces cataract. There is, however, a lack of data on the age dependence in experimental UV radiation-induced cataract.8. Microwave induced cataractMicrowave radiation has been reported to produce posterior subcapsular and cortical cataracts in rabbits and dogs within a ill-judged span of time.9. Transforming Growth Factor (TNFB) induced cataractTGFB is induced by injecting approximately 60 ng TGFB into the vitreous. TGFB induce lens epithelial cells to undergo molecular modify and abnormal morphologic that mimic the changes observed in human po sterior subcapsular and cortical cataract (Gupta, 2004).IN VITRO MODELS IN CATARACT (Gupta, 2004)Induction of cataract in isolated animal lenses well-kept in organ civilisation has become a convenient, quick and appropriate method for psychometric testing the anticataract faculty of an agent. Opacification of lens is induced by generating oxidative stress/ hyperglycemic/ hypergalactosemic conditions around the lens by supplementing the burnish fair with a variety of exogenous substances.1. Oxidative stress induced cataractOxidative mechanisms play an important aim in many biological phenomena including cataract formation. Formation of the superoxide radical in the aqueous humor, lens and its derivatization to other potent oxidants may be responsible for initiating various toxic biochemical reactions leading to the progress of cataract. In vitro such cataracts are induced by agents like selenium, H2O2, photosensitizers and enzyme xanthine oxidase.2. Selenite induced cataractI n vitro cataract is produced by supplementing the tissue culture medium with 25 to 100 mM sodium selenite in which freshly enucleated transparent rat lenses are incubated at 370C. This causes membrane damage and faint cortical opacities within 24 h.3. Photochemically induced cataractRiboflavin, a photosensitizer, is supplemented in the culture medium to induce cataract in cultured lenses. Micro quantities (4-200 M) of riboflavin lead to severe physiological damage and opacification within 24 h after exposure to light. The initial membrane damage is prove by a disturbed cation ratio between lens water and the medium of incubation. Riboflavin on getting photosensitized generates free radicals in a sequence of reactions.Lenses are maintained in organ culture for 24 to 72 h. The lenses are divided into four groups and incubated in the dark and light both in presence and absence of riboflavin. The lenses are exposed to light with two 15-w daylight fluorescent lamp placed at 8 inches ab ove the cluster plate. The culture medium is replaced every 24 h. Riboflavin shows no effect on the lens in the absence of light, and light without riboflavin has no significant effect. opacification starts in the equatorial zone and gradually extends towards the centre of the lens.4. Enzymatically induced cataractSupplementation of culture medium with 1 mM xanthine and 0.1 social unit xanthine oxidase, which act as substrate and enzyme respectively, leads to generation of superoxide radical. The lenses suffer severe oxidative damage and turn opaque within 24 h when incubated in culture medium at 370C.5. Hydrogen peroxide induced cataractIncubation of lenses in medium containing 50-500 M H2O2 and it produce cataract. Opacification starts in the equatorial region within 24 h. The entire superficial cortex becomes opaque by 96 h. Due to the high mental unsoundness of H2O2, the medium is changed every 2 h during the first eight hours.6. Sugar induced cataractTransparent and uninj ured lenses are incubated in a basis culture medium with fetal calf serum for 24 to 48 h. In the control group the medium is supplemented with glucose (30 mM), lenses develop opacity in the subcapsular region on day 1 and in the central region on day 2. Biochemical analyses reveal raised(a) polyol, malondialdehyde levels and water content, and decreased glutathione levels in these lenses.7. Steroid induced cataractSteroid-induced experimental cataract is produced in vitro by incubating the transparent lenses in the medium containing methyl prednisolone (1.5 mg/ml). The test agent and methyl prednisolone added alone and together to the medium form drug control, control and treated groups respectively. Early cataract around the equator is produced within 24 h of incubation. Incubation period may be extended to 48 h for dense opacity. Morphological changes and flection in biochemical parameters between the groups may show the potential of the anticataract agent.8. Naphthalene induc ed cataractTC-199 medium is used for the preincubation of lens. source solution of napthalene dihydrodiol is prepared in 20% ethanol at 2.5-10-3 M concentration. The stock solution is weaken 1100 to obtain the final concentration of 25.5 -10-5 M. The final osmolarity of the solution is 295-300 m Osmol. Rat lenses are incubated in TC-199 medium containing napthalene metabolite solution. Medium is renewed daily till 72 h. Lenses remain clear during the initial 24 h but from shell-like opacity around the nucleus by 48 h. Opacification becomes more skirting(prenominal) and widespread after 72 h. At 48 h, under such conditions of incubation, development of opacity mimics the in vivo napthalene cataract. Naphthalene is oxidized in the liver first to an epoxide and then is altered into naphthalene dihydrodiol. This stable component on reaching the eye gets converted enzymatically to dihydroxynaphthalene. Being unstable at physiological pH, 1,2 dihydroxynapthalene sponaneously auto oxidi ses to 1,2 naphthoquinone and H2O2. It alkylates proteins glutathione and amino acids and generates free radicals. There is a loss of protein thiol in this reaction and the products are less easily digestible by pancreatin than normal lens protein (Rees and Pirie, 1967).9. Ca2+ induced cataractIn this model, the control group contains the lenses incubated in the medium enriched with 20 mM Ca2+ or 1x 10-2 mM A23187 calcium ionopore. The treatment group lenses are cultured in the calcium and the test drug-containing medium. Incubation period can range from 24-72 h (Gupta, 2004).Fig.6 Mechanism of action of glucose-induced cataractCUsersDHINESHDesktopUntitled 7.pngUnder physiological conditions, glucose is metabolized through the glycolytic pathway. An excess amount of glucose is converted to sorbitol by enzyme aldose reductase via polyol pathway. The glucose conversion into sorbitol by utilizing NADPH results in the reduction of NADPH/NADP+. Moreover, sorbitol undergoes oxidation to fructose by using sorbitol dehydrogenase (SD). Sorbitol does not easily cross cell membrane. Intra lenticular accumulation of sorbitol, leads to lens damage (Kyselova, 2004).Fig.7 Biomorphological changes during cataract formationCUsersDHINESHDesktopUntitled 66.pngAs, the lens starts to swell in response to the hyper osmotic make of polyol accumulation, membrane permeability changes resulting in an increase in lenticular sodium and decrease in the levels of lenticular potassium, reduced glutathione, ATP and free amino acids. The overall antioxidant status of the lens decreases because of depletion of GSH (Kyselova, 2004).Mechanism of action of calcium-induced cataractFig.8 atomic number 20 transport pathwayIncreased levels of lenticular calcium activate calcium dependent proteases. The activated proteases hydrolyze cytoskeletal proteins and lens crystalline. Crystalline cleavage would result from lower molecular weight peptides that could, in turn, aggregate to form higher molecul ar weight proteins (Wang et al., 1996).Various methods for the prevention of cataractThe development of newer drugs for treatment of cataract mainly aims, interacting at the level of changed lens metabolism and lens pathophysiology. The in vitro, in vivo studies are used to identify the anti cataract agents. This epidemiologic studies may be widely classified in the following categories (Gupta et al., 1997).Aldose reductase inhibitorsAgents acting on glutathioneNonsteroidal anti -inflammatory drugsVitamins, minerals and antioxidantsMiscellaneous agents.1) Aldose Reductase InhibitorsThese drugs are aimed to prevent the metabolic dysfunctions of diabeties by polyol pathways. Aldose reductase inhibitors prevents the accumulation of sorbital within the lens would have an osmotic effect bringing in water and causing swelling and opacification. Sorbinil a spirohydantoin became the most powerful sorbitol minatory agent. Sorbinil prevents increased fluorescence and protein aggregation and it also acts as an antioxidant.2) Non Steroidal Anti inflammatory DrugsThe NSAIDS broadly studied are paracetamol, aspirin, Ibuprofen, sulindac, naproxen, and bendazec. The NSAIDS provide adequate productive effect to lens protein through various steps like acylation, carbamylation and inhibition of glycocylation. Some of them are also reported to inhibit lens AR to varying extent. NSAIDS contains antioxidant properties also. Most of the studies on the evaluation of anticataract potential of drugs have been conducted by feeding the drugs by oral route.3) Agents which act on glutathioneGlutathione is a tripeptide thiol known to control calcium inflex and protect lens protein from various agents like glucose and galactose. With advancing of age in that respect is a considerable decrease in the concentration of glutathione and the decrease more prominent in lens with cataract.4) Vitamins, minerals and antioxidantsIf oxidation in lens leads to cataract formation, then is feasible to pr event it by the use of antioxidants such as vitamins C and E and perhaps -carotene. The potential role of vitamins and antioxidants in preventing various diseases is well documented there are reports suggesting beneficial effect of vitamins like C and E in preventing cataract. Beta -carotene has also been show to protect lens damage by hematoporphysin. Ascorbate protects rubidium uptake against free radical damage and prevents light induced protein cross linking. Protective effect of vitamin C has been also reported in various in vitro studies. Vitamin E has been found to delay cataractogenesis in diabetic rats and in Emory mouse. Vitamins C and E, - Carotene and other anticataract agents belike act via a common mechanism of their scavenging properties of free radicals (Gupta et al., 1997b).Antioxidant enzymes1) Superoxide Dismutase (SOD)SODs are a family of metalloenzymes that transfer superoxide in to hydrogen peroxide (H2O2) and represents the first line of defence against oxyge n toxicity.2O2- + 2H H2O2 + O2Three isoforms of SOD have been found. The first is mainly found in the cytoplasm of cells and it containing Cu and Zn at its active site (Cu/Zn SOD-1), the second containing Mn at its active site is located in mitochondria (Mn SOD-2) and the third (Cu/Zn SOD-3) is present in the extracellular fluid like plasma. SOD is a stress protein which is synthesized mostly in response to oxidative stress. It is found that little amount of Cu, Zn and Mn metals are crucial for maintaining the antioxidant activity of SOD (Halliwell, 1994 Ray and Husain, 2002).2) Glutathione Peroxidase (GPx)GPx is one of the most important enzymes responsible for the degradation of organic peroxides and hydrogen peroxide in the brain. GPx catalyse the oxidation of GSH to GSSG at the expense of H2O2. There are two isoforms have been identified, selenium-dependent which is highly active towards H2O2 and organic hydroperoxides and selenium independent GPx. GPx activity has been reduced in selenium deficiency (Muller et al., 1984 parole et al., 2007).3) Catalase (CAT)It is a haemitin-containing protein present in most cells.2H2O2+ 2H2O O2Catalase is 104 times faster than GPx. It is having four protein subunits, each containing a heme Fe (III)-protoporphyrin group bound to its active site. GPx and CAT were found to be important in the deactivation of many environmental mutagens (Ray and Husain, 2002).4) Glutathione (GSH)GSH has major intracellular antioxidant molecule and it is a tripeptide synthesised by enzymatic reaction involving two molecules of ATP from aminoacids like glutamate, glycine and cysteine. It plays a very crucial role in detoxification of peroxides and electrophilic toxins, mainly by acting as a substrate for GSH transferase and GSH peroxidase. It was shown that weakening of GSH enhances cerebral ischemic injury in rats (Mizui et al., 1992 boy et al., 2007).