alexa Protective Effect of Epigallocatechin Gallate on Fluori
e-ISSN: 2322-0139 p-ISSN: 2322-0120

Research & Reviews: Journal of Pharmacology and Toxicological Studies
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Research Article

Protective Effect of Epigallocatechin Gallate on Fluoride-Induced Oxidative Stress Related Haematotoxicity in Rats

S Miltonprabu* and S Thangapandiyan

Department of Zoology, Faculty of Science, Annamalai University, Annamalai Nagar - 608002, Tamil Nadu, India.

*Corresponding Author:
S Miltonprabu
Department of Zoology, Faculty of Science, Annamalai University, Annamalai Nagar - 608002, Tamil Nadu, India
Tel: +91 04144 – 238282
Mobile : +91 9842325222
Fax: +91 04144 – 238080

Received date: 02 September 2013 Accepted date: 24 September 2013



Fluoride (Fl) is a naturally occurring electro negative compound which is classified as potent toxicant and human carcinogen. Erythrocytes are very expedient model to understand the susceptibility of oxidative stress on membrane induced by different xenobiotics. Fl administration (25mg/kg/BW) significantly increased the percentage of hemolysis, lipid peroxidation markers such as thiobarbituric acid reactive substances (TBARS), conjugated dienes (CD), protein carbonyls contents (PC), and altered haematological parameters, with decreased antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX),glutathione-s-transferase (GST), glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (G6PD). The levels of non-enzymic antioxidants (reduced glutathione, vitamin ‗C‘ and vitamin ‗E‘) and membrane bound ATPases (Na+/K+-ATPase, Mg2+-ATPase and Ca2+-ATPase) were also decreased in F treated rats. Pre oral administration of EGCG (40mg/k/BW) along with Fl for 28 days significantly reduced the levels of TBARS, CD and PC with significantly increased membrane ATPases, membrane integrity, viability, enzymatic and non-enzymatic antioxidants in the RBC‘s of Fl treated rats. In conclusion, the results clearly indicate that EGCG significantly attenuated the Fl induced haematotoxicity in rats.


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