Enzymatic toxicity induced by lead acetate and its possible reversal by

Abstract

Objective: An important part of male infertility of unknown etiology may be attributed to various environmental and occupational exposures to toxic substances, such as lead. Lead is the known environmental contaminant adversely affecting the male reproductive system in human and experimental animals. The cytotoxic effects of lead on male reproductive system involve the production of reactive oxygen species (ROS) and oxidative damage in tissue. The higher quantities of ROS in testicular tissue detrimentally affected enzymatic activities so as to produce verities of biochemical abnormalities and finally reduced sperm count. Methods: Adult male mice were divided into three groups: control, treated with lead acetated (1.25 mg/kg/day) and recovery group lead acetated (1.25 mg/kg/day) with vitamin E (2 mg/kg/day). Treatments were administered by daily gavage for 45 days. After treatment testis and epididymal weights were recorded and testis was used for the biochemical analysis (acid phosphatase (ACPase), alkaline phosphatase (ALKPase), and glutathione (GSH) and epididymal was used to count sperm. Results: Administration of lead acetate at a dose of 1.25mg/kg body weight for 45 days decreased the activities of all above parameters. Lead exposure resulted in oxidative stress and this was well extrapolated from the increase in lipid peroxidation products (LPP). Coadministration of vitamin E (2 mg/kg/day) with lead acetate restored all the parameters cited above to near the control values. Conclusions: This concludes that vitamin E has beneficial effects against lead acetate induced enzymatic toxicity in testicular tissue of mice.