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Mercuric chloride (HgCl(2)) has been shown to affect the male reproductive organs, and oxidative stress has been linked with hypospermatogenesis and with male infertility. However, the specific mode of impairment of spermatogenesis during HgCl(2) exposure has not yet been clarified fully. Because of the involvement of 17β-estradiol (E2) in the male reproductive tract and its putative role on spermatogenesis, the present study aimed to investigate the possibility that HgCl(2)-induced oxidative stress-mediated modulation of the E2 level exerts adverse effects on testicular steroidogenic and gametogenic activities. HgCl(2) treatment at 50 and 100 ppm for 90 days by continuous oral administration in the drink water resulted in significant dose-dependent fashion decrease in serum and testicular E(2) levels and an increase in testicular testosterone levels in dose-dependent manner, without statistical alteration in serum testosterone level among HgCl(2) exposed groups compared to the control. Cauda epididymal sperm count and motility were decreased significantly (p < 0.01), in a dose-dependent manner, in the HgCl(2)-treated groups, and qualitative examination revealed inhibition of spermatogenesis and the preferential loss of maturing and elongated spermatids. The seminiferous tubules were dilated in treated animals. When compared to the control, increase in lipid peroxidation due to toxic effects of HgCl2 was accompanied by significant reduction (p < 0.01) in antioxidant enzymes activities, superoxide dismutase, catalase, and glutathione peroxidase of testes, implicating the presence of oxidative tissue damage. Furthermore, these tissue injuries caused functional impairment as evidenced with testicular elevated activity of lactate dehydrogenase. Unless oxidative stress can lead to cancer development, testis' tumor markers as beta human chorionic gonadotropin and alpha-fetoprotein levels have shown no significant differences in the HgCl(2)-exposed group compared with respect to the control. Large quantities of metal accumulated in the testis tissue are in agreement with the testis-activity failure verified in this tissue. These findings suggest that a decrease in E2 level after mercury exposure may render testis more susceptible to oxidative damage leading to its functional inactivation, thus providing new dimension to mechanisms underlying heavy metal-induced male infertility.