Effect of lead and cadmium co-exposure on testicular steroid metabolism and antioxidant system of adult male rats

The mechanism of testicular toxicity of lead (Pb) and cadmium (Cd) is poorly understood. Previous studies focused on single metal-related changes in testicular toxicity. This study points towards the possible involvement of Pb- and Cd-induced oxidative stress in the suppression of steroidogenesis. The oxidative status of testis of adult male rats exposed to Pb acetate and cadmium acetate either alone or in combination at a dose of 0.025mgkg ^-1 body weight of metal intraperitoneally for 15days was studied. Pb and Cd caused an increase in reactive oxygen species (ROS) by elevating testicular malondialdehydes (MDA) and decrease in activities of testicular antioxidant enzymes superoxide dismutase (SOD), catalase, glucose 6 phosphate dehydrogenase (G6PDH) and glutathione-S-transferase (GST) in mitochondrial and/or post-mitochondrial fraction. Activities of steroidogenic enzymes 3β and 17β-hydroxysteroid dehydrogenase also decreased significantly leading to altered testosterone production. Metal-exposed groups showed significantly decreased testicular and epididymal sperm count. Epididymal sperm motility and viability was also decreased on Pb and Cd exposure. Cd exposure showed more toxic effect than lead exposure, while combined exposure demonstrated least toxicity. In vitro experiments showed that vitamin C restores steroidogenic enzyme activities, suggesting that Pb- and Cd-induced ROS inhibits the testicular steroidogenesis.