Laboratory of Animal Ecophysiology, Faculty of Sciences, University of Sfax, P.O. Box 802, 3018 Sfax, Tunisia.
Biol Trace Elem Res. 2011 Sep;142(3):598-610. doi: 10.1007/s12011-010-8774-2. Epub 2010 Sep 7.
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.
氯化汞（HgCl(2)）已被证明会影响男性生殖器官，氧化应激与精子生成减少和男性不育有关。然而，HgCl(2)暴露导致精子发生损伤的确切模式尚未完全阐明。由于 17β-雌二醇（E2）参与男性生殖道及其在精子发生中的潜在作用，本研究旨在探讨 HgCl(2)诱导的氧化应激介导的 E2 水平调节是否对睾丸甾体生成和配子发生活动产生不利影响的可能性。通过连续口服饮用水中的 50 和 100 ppm HgCl(2)处理 90 天，导致血清和睾丸 E(2)水平呈显著剂量依赖性下降，睾丸睾酮水平呈剂量依赖性增加，与对照组相比，HgCl(2)暴露组的血清睾酮水平没有统计学变化。尾附睾精子计数和活力显著下降（p<0.01），呈剂量依赖性，HgCl(2)处理组精子发生受到抑制，成熟和伸长精子优先丢失。睾丸曲细精管扩张。与对照组相比，HgCl2 的毒性作用导致脂质过氧化增加，同时睾丸抗氧化酶超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶的活性显著降低（p<0.01），提示存在氧化组织损伤。此外，这些组织损伤导致功能障碍，如睾丸乳酸脱氢酶活性升高。除非氧化应激能导致癌症发展，否则睾丸肿瘤标志物β人绒毛膜促性腺激素和α-胎蛋白水平在 HgCl(2)暴露组与对照组相比没有显著差异。大量金属在睾丸组织中的积累与该组织中验证的睾丸活性衰竭一致。这些发现表明，汞暴露后 E2 水平下降可能使睾丸更容易受到氧化损伤，导致其功能失活，从而为重金属诱导的男性不育的机制提供了新的维度。
