Cadmium is an environmental and industrial pollutant that affects the male reproductive system of humans and animals. However, the mechanism of its adverse effect on Leydig cell steroidogenesis remains unknown. The present study points to the possible involvement of oxidative stress in the suppression of steroidogenesis. Cadmium administration caused an increase in reactive oxygen species (ROS) by elevating testicular malondialdehyde (MDA) and decreasing the activities of testicular antioxidant enzymes such as glutathione peroxidase and superoxide dismutase. The mRNA of Steroid Acute Regulatory (StAR) protein was substantially reduced. The activities of testicular delta5-3beta and 17-beta-hydroxysteroid dehydrogenases (HSD) as well as serum testosterone level were also lowered, suggesting that cadmium-induced ROS inhibit testicular steroidogenesis. Supplementation with vitamin C (VC) and or vitamin E (VE) reduced testicular ROS and restored normal testicular function in Cd-exposed rats. We conclude that VC and VE prevent oxidative stress and play vital roles in co-regulating StAR gene expression and steroid production in cadmium-exposed rats.