The unfavourable outcome of cadmium (Cd) on male fertility, sex hormones' production and sperm criteria have been reported in literature (Medina et al., 2017). Testicular tissue is particularly susceptible to cadmium-induced damage. Cd causes degeneration of rats' epididymis, seminal vesicles and spermatozoa (Sajjad et al., 2014). Cd, other heavy metals and oestrogenic-based compounds may explain the recent deterioration in male fertility in industrialised regions in the form of sperm count and testicular function reduction. This may involve the fact that Cd disrupts endocrine control of testicular tissue and induces oxidative damage (Siu et al., 2009). Cd exposure is linked with the generation of free radicals in acute toxicity and reactive oxygen species (ROS) in chronic toxicity. Cdgenerated superoxide anion, hydrogen peroxide and hydroxyl radicals have been reported and are usually associated with redox reactions and ROS-related genetic alterations. It is, therefore, stated that oxidative damage plays an integral part in cadmium toxicity (Liu et al., 2009). In rats subjected to prenatal Cd exposure, plasma testosterone concentrations are drastically lowered and expression of