Introduction: In early 1960s, there is a first evidence of the toxic effects ionizing radiation on elevated oxygen levels in aerobes and proposed that oxygen toxicity is due to free radical formation. An alteration between oxidants and antioxidants in favour of the oxidants, potentially leading to damage is termed oxidative stress. Lead and cadmium do not have any detectable beneficial biological roles rather it produces detrimental effects on biochemical, physiological and behavioral dysfunctions. Even a little lead poisoning can cause serious health problems, and at very high levels, it can be fatal. Mainly it affects the heamopoeitc system, Liver, Kidney, Cardiovascular system and reproductive system. Methodology: Experimental rats, injected intraperitoneally with lead acetate for 15 days at the dosage of 50, 100 mg/kg/day body weight and compared to control rats injected with deionized distilled water instead. At the end of study testis were removed and right testis was used for testicular antioxidant Malandealdehyde (MDA) levels estimation by Thiobarbituric acid reactive substance assay and left testis was used for histopathological analysis. Unpaired t test and ANOVA was used for statistical analysis. Results : The MDA (nmole /gm tissue) levels in control, lead 50mg, lead 100mg groups were 12.16±0.4, 17.06±0.16 and 18.11±0.13. Histopathology examination Lumen showing decreased sperm count and maturation. Some of the lumens showing absence sperm maturation. Conclusion: Study on lead-exposed rat testis have shown that reduction of spermatogenesis formation and sperm maturation. Increased MDA levels indicate that it may be due to oxidative stress. The toxicity of lead was noted at level ≥50mg/kg.
Lead;Lipid peroxidation;Male reproduction;Testicular histology