HEPATOTOXIC AND NEPHROTOXIC EFFECTS OF SODIUM SELENITE IN RATS

1. HEPATOTOXIC AND NEPHROTOXIC EFFECTS OF SODIUM SELENITE IN RATS Bogdan Gabriel Şlencu1, Carmen Solcan2, Liliana Avasilcăi1, Rodica Cuciureanu1 1School of Pharmacy, “Grigore T. Popa” University of Medicine and Pharmacy Iași, Romania 2 School of Veterinary Medicine, “Ion Ionescu de la Brad” University of Agricultural Sciences and Veterinary Medicine, Iași, Romania INTRODUCTION AND OBJECTIVES MATERIAL AND METHOD RESULTS REFERENCES CONCLUSIONS Selenium is an essential microelement. In high doses it is generally toxic, both for animals and humans (Reilly, 2006). Elemental selenium is considered to be almost biologically inert (Zhang et al, 2005), due to insolubility. Inorganic salts, such as selenite and selenate, are very toxic (National Toxicology Program, 1994). Organic compounds of selenium, such as selenomethionine, are less toxic than the inorganic ones (Reilly, 2006; Schrauzer, 2000). Selenitecan react intracellulary or extracellularly with glutathione (Mezes et Balogh, 2009). The objective of this study was to investigate and compare the subacute toxicity of sodium selenite administered by oral route at two different doses, in male rats. Seleniteinterfered with the growth gain and caused an increase in ALT, AST and GGT activities and in the levels of total and direct bilirubin, serum iron, total cholesterol, HDL-cholesterol and LDL-cholesterol (Table I). Selenite caused a decrease in WBC and RBC numbers and in HGB concentration (Table II). In the two selenite groups hydropic degeneration, perivascular edema, cells with apoptotic bodies, intensely acidophilic cells with picnotic nuclei, oval cells, necrosis and anuclear cells were observed in the livers (Table III, Table IV). Hydropic degeneration, intensely acidophilic cells with picnotic nuclei, hyaline cylinders, congestion, vascular ectasia and perivascular edema were observed in the kidneys. Male Wistar rats were used, which were randomly divided in one of the three experimental groups consisting in 5 rats each: Control, Se1 (1 mg Se+4 equivalent/kg body weight) and Se3 (3 mg Se+4 equivalent/kg body weight). All treatments were administered once a day for 10 consecutive days and the animals were sacrificed on the 11th day. The following biochemical parameters were determined from serum: alaninetransaminase (ALT), aspartatetransaminase (AST), serum iron, total bilirubin, direct bilirubin, gamma glutamyltranspeptidase (GGT), total cholesterol, HDL-cholesterol, LDL-cholesterol, serum urea, serum creatinine, serum uric acid. A full blood count was performed. Liver and kidney sections were stained with hematoxylin and eosin (HE technique) and analyzed. These data indicate a dose-dependent effect of sodium selenite on pathological changes in biochemical parameters and in histological architecture. Oval cells were significantly present only in the livers of the rats receiving the highest dose of selenite (3 mg Se+4/kg body weight). At the lowest dose it could be possible that the induced hepatic histopathological changes could be reversible. • Mezes M, Balogh K. Prooxidant mechanisms of selenium toxicity - a review. Acta BiologicaSzegediensis2009; 53:15-18. • National Toxicology Program. NTP technical report on toxicity studies of sodium selenate and sodium selenite administered in drinking water to F344/N rats and B6C3F1 mice, In: Toxicity Report Series No. 38. NIH Publication 94-3387, Bethesda, Maryland: National Institutes of Health, 1994. • Reilly C. Selenium in food and health, 2nd edition. New York: Springer, 2006. • Schrauzer GN. Selenomethionine: a review of its nutritional significance, metabolism and toxicity. J Nutr 2000; 130:1653-1656. • Zhang J, Wang H, Yan X, Zhang L. Comparison of short-term toxicity between Nano-Se and selenite in mice. Life Sci2005; 76: 1099-1109. Table III. Hepatic lesions in the Se1 group Table IV. Hepatic lesions in the Se3 group Table I. Effect of sodium selenite on some biochemical parameters Table II. Effect of sodium selenite on some haematological parameters