Lee I P, Dixon R L
J Pharmacol Exp Ther. 1975 Jul;194(1):171-81.
Recently the potential toxicity of environmental mercury has become a major concern. Human tissues contain mercury due to daily environmental exposure. Nearly all of the mercury contaminating food is in the form of methylmercury complexes, due to the biotransformation of inorganic mercury. This report compares the reproductive effects of methylmercury hydroxide and mercuric chloride in male mice. The mercuric compounds were administered intraperitoneally once at a dose of 1 mg/kg (based on Hg++ concentration), or spermatogenic cells were exposed in vitro to Hg+ concentrations ranging from 10(-3) to 10(-8)M. Spermatogenic cells were separated for biochemical studies using the velocity sedimentation technique, and in vivo serial mating was used to assess fertility. The effects of CH3Hg+ or Hg++ on the uptake of 3H-thymidine by spermatogonia, 3H-uridine by early elongated spermatids, and 3H-L-leucine by late elongated spermatids were studied. These in vitro experiments indicated that at 1-(-3) m CH2HgOH reduced thymidine incorporation by spermatogonia by 40%, uridine incorporation by elongated spermatids by 39% and L-leucine incorporation by late elongated spermatids by 40%. Results obtained with HgCl2 were similar but of lesser magnitude. In vivo administration of CH3HgOH and HgCl2 significantly inhibited the uptake of thymidine, uridine and L-leucine by their respective spermatogenic cells. Fertility profiles obtained from serial mating studies indicated that the primary effect of CH3HgOH was on spermatogonial cells, premeiotic spermatocytes and early elongated spermatids, with no apparent effect on spermatozoa in testis, peididymis or vas deferentia. HgCl2 also primarily affected spermatogonial and premeiotic cells, but the effect was less than that seen with CH3HgOH. Statistical analysis indicated significant antifertility effects. Inhibition of uptake of thymidine and uridine was well correlated with the functionality of these cells as reflected in the fertility profile, excep for L-leucine uptake. Mercury ion-induced antifertility effects at the dosage used in these experiments are reversible. Thus, these results suggest spermatogenic effects of methylmercury complexes which might have important health consequences in man.
最近，环境汞的潜在毒性已成为一个主要问题。由于日常环境暴露，人体组织中含有汞。由于无机汞的生物转化，几乎所有污染食物的汞都是甲基汞络合物的形式。本报告比较了氢氧化甲基汞和氯化汞对雄性小鼠的生殖影响。汞化合物以1mg/kg的剂量（基于Hg++浓度）腹腔注射一次，或者将生精细胞在体外暴露于浓度范围为10(-3)至10(-8)M的Hg+中。使用速度沉降技术分离生精细胞用于生化研究，并通过体内连续交配来评估生育能力。研究了CH3Hg+或Hg++对精原细胞摄取3H-胸腺嘧啶核苷、早期伸长型精子细胞摄取3H-尿苷以及晚期伸长型精子细胞摄取3H-L-亮氨酸的影响。这些体外实验表明，在10(-3)m时，CH2HgOH使精原细胞的胸腺嘧啶核苷掺入减少40%，伸长型精子细胞的尿苷掺入减少39%，晚期伸长型精子细胞的L-亮氨酸掺入减少40%。用HgCl2获得的结果相似，但程度较小。体内给予CH3HgOH和HgCl2显著抑制了各自生精细胞对胸腺嘧啶核苷、尿苷和L-亮氨酸的摄取。从连续交配研究获得的生育情况表明，CH3HgOH的主要作用是对精原细胞、减数分裂前的精母细胞和早期伸长型精子细胞，对睾丸、附睾或输精管中的精子没有明显影响。HgCl2也主要影响精原细胞和减数分裂前的细胞，但其作用小于CH3HgOH。统计分析表明有显著的抗生育作用。胸腺嘧啶核苷和尿苷摄取的抑制与这些细胞在生育情况中反映的功能密切相关，但L-亮氨酸摄取除外。在这些实验中使用的剂量下，汞离子诱导的抗生育作用是可逆的。因此，这些结果表明甲基汞络合物对生精有影响，这可能对人类健康产生重要后果。
