Ascorbic acid attenuates lead-induced oxidative stress and testosterone suppression in male Wistar rats.

OBJECTIVES

Lead (Pb) exposure is a major environmental risk factor for male reproductive dysfunction, primarily mediated through oxidative stress and endocrine disruption. This study evaluated the effects of lead acetate on testicular antioxidant status and serum testosterone levels and investigated the ameliorative role of ascorbic acid (AA) in adult male Wistar rats.

METHODS

Thirty-five male Wistar rats were randomly assigned to seven groups (n=5): control, low- and high-dose lead (100 and 200 mg/kg), lead plus AA cotreatment, and withdrawal groups. Testicular antioxidant enzymes (SOD, CAT, GPx), reduced glutathione (GSH), and malondialdehyde (MDA) were assessed spectrophotometrically. Serum testosterone was measured using enzyme immunoassay. Data were analyzed using one-way ANOVA (p<0.05).

RESULTS

Lead exposure significantly increased MDA levels and reduced antioxidant enzyme activities and testosterone concentrations in a dose-dependent manner (p<0.05). Ascorbic acid coadministration significantly restored antioxidant status, elevated GSH levels, reduced lipid peroxidation, and improved testosterone levels compared with lead-only and withdrawal groups.

CONCLUSIONS

Lead acetate induces oxidative and endocrine disturbances in testicular tissue. Ascorbic acid effectively mitigates lead-induced reproductive toxicity by preserving antioxidant defenses and maintaining testosterone homeostasis.