STATUS OF ENZYMATIC ANTIOXIDANTS IN EYE LENS EXTRACTED FROM CATARACTOUS SUBJECTS
Keywords:cataractous lens, Enzymatic antioxidants, Cataractous subjects, Apparently normal, diabetic, Hypertensive
Objectives: Cataract is a common kind of blindness prevailing in India. Eye lens is normally exposed to toxic elements of the surroundings, leading to the formation of free radicals. In normal conditions, the presence of antioxidants may help to counteract the progression of free radical formation in an eye lens. Hence, it was requisite to assess the activities of enzymatic antioxidants in the eye lens extracted from cataractous subjects.
Methods: The cataractous lens samples of 120 subjects were collected from the ophthalmic centres in and around Coimbatore. The subjects were categorised into apparently normal cataract men (ACM), apparently normal cataract women (ACW), diabetic cataract men (DCM), diabetic cataract women (DCW), hypertensive cataract men (HCM) and hypertensive cataract women (HCW) with each group consisting of 20 samples. Activities of enzymatic antioxidants namely superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST) were assessed in the cataractous lens samples from the selected subjects. Data was interpreted using SPSS 16.0 software package.
Results: The activities of SOD and CAT were found to be significantly decreased (p<0.05) in all the five groups when compared to apparently normal cataract men. Enzymes of glutathione system exhibited a significant variation (p<0.05) in their activity in the cataractous eye lens extracted from diabetic and hypertensive cataract women in comparison to apparently normal cataract men. A significant decrease (p<0.05) in the activities of GR and GST was also observed in the cataractous eye lens extracted from diabetic and hypertensive cataract men when compared to the subjects of ACM group.
Conclusion: The outcome of the study suggested that cataractous subjects with clinical complications were much disposed to the reactive oxygen species and more affected than the apparently normal cataractous subjects.
Asbell PA, Dualan I, Mindel J, Brocks D, Ahmad M, Epstein S. Age-related cataract. Lancet 2005;365:599-609.
Schaumberg DA, Glynn RJ, Christen WG, Ajani UA, Sturmer T, Hennekens CH. A prospective study of blood pressure and risk of cataract in men. Ann Epidemiol 2001;11:104-10.
Younan C, Mitchell P, Cumming R, Rochtchina E, Panchapakesan J, Tumuluri K. Cardiovascular disease, vascular risk factors and the incidence of cataract and cataract surgery: the Blue Mountains Eye Study. Ophthalmic Epidemiology 2003;10:227-40.
Tang PH, Kono M, Koutalos Y, Ablonczy Z, Crouch RK. New insights into retinoid metabolism and cycling within the retina. Prog Retinal Eye Res 2013;32:48-63.
Tiwari AK. Antioxidants: New-generation therapeutic base for treatment of polygenic disorders. Curr Sci 2004;86(8):1092-102.
Roche M, Rondeau P, Singh NR, Tarnus E, Bourdon E. The antioxidant properties of serum albumin. FEBS Lett 2008;582(13):1783-7.
Angaji SA, Mousavi SF, Babapour E. Antioxidants: A few key points. Ann Biol Res 2012;3(8):3968-77A.
Gul A, Rahman MA, Hasnain SN, Salim A, Simjee SU. Could oxidative stress associate with age-products in cataractogenesis? Curr Eye Res 2008;33(8):669-75.
Virgolici B, Stoian I, Muscurel C, Maracine M, Moraru C, Dinu V. Plasma redox status and premature onset of senile cataract. Rom J Intern Med 2007;45:59-65.
Cekic G, Zlatanovic G, Cvetkovic T, Petrovic B. Oxidative stress in cataractogensis. Bosnian J Basic Med Sci 2010;10(3):265-9.
Harocopos GJ, Shui YB, McKinnon M, Holekamp NM, Gordon MO, Beebe DC. Importance of vitreous liquefaction in age-related cataract. Invest Ophthalmol Visual Sci 2004;45:77-85.
Barnett M, Lin D, Akoyev V, Willard L, Takemoto D. Protein kinase C epsilon activates lens mitochondrial cytochrome c oxidase subunit IV during hypoxia. Exp Eye Res 2008;86:226-34.
Fridovich I. Superoxide anion radical (O2.-), superoxide dismutases, and related matters. J Biol Chem 1997;272:18515-7.
Ho YS, Xiong Y, Ma W, Spector A, Ho DS. Mice lacking catalase develop normally but show differential sensitivity to oxidant tissue injury. J Biol Chem 2004;279:32804-12.
John M, Jaworski C, Chen Z, Subramanian S, Ma W, Sun F, et al. Matrix metalloproteins are down-regulated in rat lenses exposed to oxidative stress. Exp Eye Res 2004;79:839-46.
Ma W, Nunes I, Young CS, Spector A. Catalase enrichment using recombinant adenovirus protects alpha TN4-1 cells from H2O2. Free Radic Biol Med 2006;40:335-40.
Deponte M, Urig S, Arscott LD, Fritz-Wolf K, Reau R, Herold-Mende C, et al. Mechanistic studies on a novel, highly potent gold-phosphole inhibitor of human glutathione reductase. J Biol Chem 2005;280:20628-37.
Karplus PA, Schulz GE. Substrate binding and catalysis by glutathione reductase as derived from refined enzyme: Substrate crystal structures at 2 A resolution. J Mol Biol 1989;210:163-80.
Schulz GE, Schirmer RH, Sachsenheimer W, Pai EF. The structure of the flavoenzyme glutathione reductase. Nature 1978;273:120-4.
Beauchamp C, Fridovich I. Superoxide dismutase: improved assays and an assay applicable to acrylamide gels. Anal Biochem 1971;44:276-87.
Luck H. In: Methods in enzymatic analysis, 2 (Ed. Bergmeyer), Academic Press: New York; 1974. p. 885.
Rotruck JT, Pope AL, Ganther HE, Swanson AB, Hafeman DG, Hekstra WG. Selenium biochemical role as a component of glutathione peroxidase, purification and assay. Sci 1973;179:588-90.
Habig WH, Pabst MJ, Jakoby WB. Glutathione S-transferases, The first enzymatic step in mercapturic acid formation. J Biol Chem 1974;249:7130â€“9.
Beutler E. Red cell metabolism: a manual of biochemical methods, Orlando FL: Grune and Stratton; 1984. p. 68-73.
Bron AJ, Brown NAP, Harding JJ, Ganea E. The lens and cataract in diabetes. Int Ophthalmol Clin 1998;38:37-67.
Sobti S, Sahni B. Cataract among adults aged 40 years and above in a rural area of Jammu district in India: Prevalence and risk-factors. IJHBR 2013;1(4):284-96.
Hashim Z, Zarina S. Antioxidant markers in human senile and diabetic cataractous lenses. J College Physicians Surgeons Pakistan 2006;16:637-40.
Donma O, Yorulmaz E, Pekel H, Suyugul N. Blood and lens lipid peroxidation and antioxidant status in normal individuals, senile and diabetic cataractous patients. Curr Eye Res 2002;25:9-16.
Fujiwara H, Takigawa Y, Suzuki T, Nakata K. Superoxide dismutase activity in cataractous lenses. Jpn J Ophthalmol 1992;36:273-80.
Rieger G, Winkler R. Changes of glutathione peroxidase activity in eye tissues of Emroy mice in relation to cataract status and age. Opthalmologica 1994;208:5-9.
Reddan JR, Steiger CA, Dziedzic DC, Gordon SR. Regional differences in the distribution of catalase in the epithelium of the ocular lens. Cell Mol Biol 1996;42:209-19.
Carey JW, Pinarci EY, Penugonda S, Karacal H, Ercal N. In vivo inhibition of l-buthionine-(S,R)-sulfoximine-induced cataracts by a novel antioxidant, N-acetylcysteine amide. Free Radic Biol Med 2011;50:722-9.
Barker JE, Heales SJ, Cassidy A, BolaÃ±os JP, Land JM, Clark JB. Depletion of brain glutathione results in a decrease of glutathione reductase activity: an enzyme susceptible to oxidative damage. Brain Res 1996;716:118-22.
Rao GN, Sadasivudu B, Cotlier E. Studies on glutathione S-transferase, glutathione peroxidase and glutathione reductase in human normal and cataractous lenses. Ophthalmic Res 1983;15:173-9.
Spector A, Wang GM, Wang RR, Garner WH, Moll H. The prevention of cataract caused by oxidative stress in cultured rat lenses, I. H2O2 and photochemically induced cataract. Curr Eye Res l993;12:163-79.
Spector A, Wang GM, Wang RR. The prevention of cataract caused by oxidative stress in cultured rat lenses 11. Early effects of photochemical stress and recovery. Exp Eye Res 1993;57:659-67.