Title of article :
Mercuric chloride-induced testicular toxicity in rats and the protective role of sodium selenite and vitamin E
Author/Authors :
Kalender، نويسنده , , Suna and Uzun، نويسنده , , Fatma Gokce and Demir، نويسنده , , Filiz and Uzunhisarc?kl?، نويسنده , , Meltem and Aslanturk، نويسنده , , Ayse، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2013
Pages :
7
From page :
456
To page :
462
Abstract :
Mercury has been recognized as an environmental pollutant that adversely affects male reproductive systems of animals. This study examined the effects of mercuric chloride on the antioxidant system and histopathological changes and also evaluated the ameliorating effects of sodium selenite and/or vitamin E in the rat testis tissues. Sexually mature male Wistar rats (weighing 300–320 g and each group six animals) were given mercuric chloride (1 mg/kg bw) and/or sodium selenite (0.25 mg/kg bw) + vitamin E (100 mg/kg) daily via gavage for 4 weeks. In the present study, mercuric chloride exposure resulted in an increase in the TBARS level and a decrease in the SOD, CAT, GPx activities, with respect to the control. Further, light microscopic investigation revealed that mercury exposure induced histopathological alterations in the testis tissues. Supplementation of sodium selenite and/or vitamin E to mercury-induced groups declined lipid peroxidation, increased SOD, CAT, GPx activities. While some histopathological changes were detected in mercuric chloride treated group, milder histopathological changes were observed in animal co-treated with sodium selenite and/or vitamin E supplementation to mercuric chloride-treated rats. As a result, mercuric chloride induced testicular toxicity is reduced by sodium selenite and/or vitamin E, but not ameliorate completely.
Keywords :
Mercuric Chloride , Sodium selenite , histopathology , vitamin E , oxidative stress , Testicular toxicity
Journal title :
Food and Chemical Toxicology
Serial Year :
2013
Journal title :
Food and Chemical Toxicology
Record number :
2124881
Link To Document :
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