Abstract
The present study was aimed to investigate whether α-tocopherol could protect the chromium (Cr) VI-induced oxidative stress in female reproductive system of rats and to explore the underlying mechanisms of the same. A total of 24 Wistar adult female rats were equally divided into four groups. Group 1 served as control, while groups 2 and 3 were administered K2Cr2O7 (10 mg/kg b.wt. s.c. single dose). In addition to Cr, group 3 also received α-tocopherol @ 125 mg/kg daily by oral gavage for 14 days. Group 4 was maintained as α-tocopherol control (dose as above). Body weights were recorded at the beginning and at the end of experiment. Further, the rats were observed for occurrence of estrus cycle. At the end of 14 days, blood samples were drawn for sero-biochemical analysis. Subsequently, all the rats were sacrificed to collect uterus along with ovaries for assay of tissue peroxidation, anti-oxidant and functional markers, and histopathology. Administration of chromium (Cr) VI to rats revealed a significant (P < 0.05) accumulation of cholesterol and a prolonged diestrus phase leading to impaired fertility in rats. Administration of chromium (Cr) VI significantly (P < 0.05) reduced the antioxidant markers such as superoxide dismutase (SOD) and reduced glutathione (GSH), along with significant (P < 0.05) increase in peroxidation markers such as malondialdehyde and protein carbonyls in ovaries. The functional marker in serum such as total protein was decreased, whereas other functional markers viz alanine transaminase (ALT), blood urea nitrogen (BUN) and creatinine were increased. Prominent pathological changes were observed in the uterus and ovaries of Cr-treated group. Co-treatment with α-tocopherol significantly (P < 0.05) reversed the (Cr) VI induced changes.
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