Main Article Content
BisphenolA (BPA) is an environmental contaminant with two (2) phenolic groups. It is used as plasticizer in plastic and rubber industries. Free BPA is released and it migrates into the food, beverages, as it is used as lacquer in the linning of beverage cans, its migration is enhanced by repeated washing, rubbing and sterilization. Continous exposure to BPA exerts oxidative stress effects on cells. This study investigated the possibility of total glutathione, oxidized glutathione and reduced glutathione perturbations at prevailing low exposure rates in female albino Wistar rats, following exposure for the period of three (3) months. To eleven experimental groups each containing ten (10) non-pregnant female rats were administered 0.05, 0.1, 00.2, 0.3, 0.4, 0.5, 0.6, 0.7, 0.8, 0.9, and 1 mg of BPA/kgbw/day. To the twelveth (12th) control group was given water. Blood was collected from animals at the end of every week of the study and serum sample specimens analyzed by routine diagnostic procedures for total glutathione, oxidized glutathione and reduced glutathione using Autochemical Analyzer. Significantly increased concentrations of serum total glutathione, oxidized glutathione and decreased reduced glutathione were observed at all concentrations of BPA exposure suggesting that bisphenol A upsets total glutathione, oxidized glutathione and reduced glutathione balance. Hence, inducing cellular toxicity and then apoptosis.
This work is licensed under a Creative Commons Attribution 4.0 International License.
AboulEzz, H.S., Khadrawy, Y.A. andMourad, I.M. (2015): The effect of bisphenol A on some oxidative stress parameters and acetylcholinesterase activity in the heart of male albino rats.Cytotechnology. 67(1): 145–155.
Burgoyne, J.R., Mongue-Din, H., Eaton, P. and Shah, A.M.( 2012). Redox signaling in cardiac physiology and pathology. Circulation Research, 111: 1091–1106.
Cao, J., Mickens, J.A., McCaffrey, K.A., Leyrer, S.M. and Patisaul, H.B. (2012). Neonatal bisphenol A exposure alters sexually dimorphic gene expression in the postnatal rat hypothalamus. Neurotoxicology33(1):23–36.
Carwile, J.L. and Michels, K.B. (2011). UrinarybisphenolAandobesity:NHANES 2003–2006. Environmental Research. 111:825–830.
Enzo Life Sciences Inc.(2007), 10 Executive Boulevard Farmingdale, NY 11735, email@example.com
European Food Safety Authority EFSA Panael on food contact materials,enzymes,flavoouring and processing aids (CEF), (2010): Scientific Opinion on Bisphenol A: evaluation of a study investigating its neurodevelopmental toxicity,review of recent scientific literature on it toxicity and advice on the Danish risk assessment of Bisphenol A. EFSA Journal 8(9):1829.
Fenichel, P., Chevalier, N. andBrucker-Davis, F. (2013).Bisphenol A: an endocrine and metabolic disruptor. Annals of Endocrinology, 74(3):211–220.
Hassan, Z.A., Elobeid, M.A., Virk,P., Omer,S.A., ElAmin, M., Daghestani,M.H and AlOlayan, E.M. (2012). Bisphenol A induce hepatotoxicity through oxidative stress in rat model. Oxidative Medicine and Cellular Longevity, 10: 11-55.
Husain, K. and Hazelrigg, S.R.(2002): Oxidative injury due to chronic nitric oxide synthase inhibition in rat: effect of regular exercise on the heart. Biochimical and Biophysical Acta, 1587:75–82.
Korkmaz, A., Aydogan, M., Kolankaya, D. and Barlas, N. (2010).Influnce of vitamin C on bisphenol A, nonylphenol and octyl-phenol induced oxidative damages in liver of male rats. Food and Chemical Toxicology, 48:2865-2871.
Nandi, D., Patra, R. C. and Swarup, D. (2005 ). “Effect of cysteine, methionine, ascorbic acid and thiamine on arsenic-induced oxidative stress and biochemical alterations in rats,” Toxicology, 211(1): 26–35,.
Nishikawa, M., Iwano, H., Yanagisawa, R., Koike, N., Inoue, H. and Yokota, H. (2010).Placental Transfer of Conjugated Bisphenol A and Subsequent Reactivation in the Rat Fetus. Environmental Health Perspectives,118 (9): 1196–1203.
Rubin, B.S. (2011). Bisphenol A: an endocrine disruptor with widespread exposure and multiple effects. Journal of Steroid Biochemistry and Molecular Biology, 127: 27-34.
Schönfelder, G., Wittfoht, W., Hopp, H., Talsness, C.E., Paul, M. and Chahoud, I. (2002). Parent bisphenol A accumulation in the human maternal–fetal–placental unit. Environmental Health Perspective, 110(11):A703–A707.
Sharma, R., Yang, Y., Sharma, A., Awasthi, S. and Awasthi, Y. C. (2004): Antioxidant role of glutathione S-transferases: protection against oxidant toxicity and regulation of stress-mediated apoptosis. Antioxidants and Redox Signaling, 6(2): 289–300.
Sun, H., Shen, O.X., Wang, X.R., Zhou, L., Zhen, S.Q. and Chen, T.E. (2004).Antithyroid hormone activity of bisphenolA, tetrabromobisphenol A andtetachlorobisphenol A in an improved reporter gene assay. ToxicologyIn vitro,4(3):2-5.
Vaziri, N.D., Wang, X.Q., Oveisi, F. and Rad, B. (2000). Induction of oxidative stress by glutathione depletion causes severe hypertension in normal rats. Hypertension36:142–146.
Wan, Y., Choi, K. and Kim, S. (2010). Hydroxylatedpolybrominateddiphenyl ethers and bisphenol A in pregnant women and their matching fetuses: placental transfer and potential risks. Environmental Science Technology,44(13):5233–5239.
Wu, J.H., Jiang, X.R., Liu, G.M., Liu, X.Y., He, G.L. and Sun, Z.Y. (2011). Oral exposure to low-dose bisphenol A aggravates testosterone-induced benign hyperplasia prostate in rats. Toxicology and Industrial Health,27:810-819.
Yamada,H., Yamada, I., Furuta, E.H., Kato, S. and Kataoka, Y.U. (2002).Maternal serum and amniotic fluid bisphenol A concentrations in the early second trimester. Reproductive Toxicology,16: 735-739
Yoo, S.D., Shin, B.S., Kwack, S.J., Lee, B.M., Park, K.L., Han, S.Y. and Kim, H.S. (2000). Pharmacokinetic disposition and tissue distribution of bisphenol A in rats after intravenous administration. Toxicology and Environmental Health A61:131–139.