Oral administration of cadmium depletes intratesticular and epididymal iron levels and inhibits lipid peroxidation in the testis and epididymis of adult rats.

Cadmium (Cd)-induced tissue injury depends on the accumulated Cd which differentially affects endogenous iron (Fe). To investigate this, adult rats were treated by oral gavage with Cd (50 mg/kg body wt.) once a week for 15, 30 and 60 days and sacrificed a day after last administration. After the 15th and 30th day of treatment, Cd had no effect on thiobarbituric acid reactive substances (TBARS) and endogenous Fe levels but exhibited anti-androgenic effects (p < 0.05) and caused histological damages. At day 60, Cd was accumulated by 156.30% and 364.77% above control values at concentrations that decreased endogenous Fe levels by 46.41% and 50.31% in the testis and epididymis respectively. The histological damages were characterized by decreased tubular diameter, damage to the epithelium leading to loss of tubular germ cells and absent of spermatozoa in the epididymal lumen. Although myeloperoxidase activities were increased, TBARS levels were found to decrease significantly at day 60 in the serum, testis and epididymis suggesting that the histological damages were not caused by lipid peroxidation. Furthermore, TBARS correlated negatively with Cd in the testis (r = -0.251, p < 0.05) and epididymis (r = -0.286, p < 0.05); Fe correlated positively with TBARS in the testis (r = +0.217, p < 0.05) and Cd correlated negatively with Fe in the testis (r = -0.461, p < 0.05) and epididymis (r = -0.109, p < 0.05). The antioxidant enzymes, superoxide dismutase and glutathione peroxidase were also decreased in the gonads after 60 days Cd treatment. Overall, anti-androgenic effects and histo-pathological changes are early indicators of direct effects of Cd and occur before decrease in TBARS which is secondarily related to the modifying of Fe contents.