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首页> 外文期刊>Comparative Medicine >Zinc-induced survival of Leydig cells in Fischer rats (Rattus norvegicus) treated with cadmium chloride
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Zinc-induced survival of Leydig cells in Fischer rats (Rattus norvegicus) treated with cadmium chloride

机译：锌诱导的氯化镉处理的Fischer大鼠（Rattus norvegicus）Leydig细胞的存活

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Zinc is known to prevent cadmium-induced carcinogenesis and Leydig cell destruction in rat testes; however, the mechanism of action is not known, although it has been suggested that pituitary feedback increases the production of luteinizing hormone (LH) in response to low circulating androgen. We therefore examined the biological role of zinc in reducing cadmium toxicity in the Leydig cells of Fischer rats. Two groups of eleven 6-month-old rats were injected subcutaneously with 20 micromol CdCl2/kg weekly for 5 weeks; one of these groups also received 1 mmol/kg zinc acetate weekly for the same 5 weeks. A third group of rats received 1 mmol/kg zinc acetate weekly, and a fourth group was injected with saline weekly for 5 weeks. After 8 months of study, the animals were euthanized by CO2 inhalation. The results indicated that the number of surviving Leydig cells was significantly lower in the cadmium group (7.34% = 0.095 x 10(9)/cm3) than in the cadmium-zinc group (20.85%) or control animals (91.2%). Moreover, the concentrations of serum testosterone and LH were significantly higher in the cadmium group than in any of the other groups. This difference probably was due to the testosterone produced by a small reservoir of surviving Leydig cells and to other endocrine factors. These findings suggest that Fischer rat testis may be a good model system for testing the effects of cadmium and zinc on the production of LH and testosterone and other androgens before spontaneous cancers develop.
机译：已知锌可以防止镉诱导的大鼠睾丸癌变和Leydig细胞破坏。然而，尽管已经提出垂体反馈可响应低循环雄激素而增加黄体生成激素（LH）的生成，但其作用机理尚不清楚。因此，我们研究了锌在降低Fischer大鼠Leydig细胞中镉毒性中的生物学作用。两组11只6月龄大的大鼠每周皮下注射20微摩尔CdCl2 / kg，持续5周。这些组中的一组在相同的5周内也每周接受1 mmol / kg乙酸锌。第三组大鼠每周接受1 mmol / kg醋酸锌，第四组大鼠每周注射盐水5周。研究8个月后，通过吸入二氧化碳使动物安乐死。结果表明，镉组的存活Leydig细胞数量（7.34％= 0.095 x 10（9）/ cm3）显着低于镉锌组（20.85％）或对照动物（91.2％）。此外，镉组的血清睾丸激素和LH浓度显着高于其他任何组。这种差异可能是由于少量存活的Leydig细胞库产生的睾丸激素和其他内分泌因素引起的。这些发现表明，Fischer大鼠睾丸可能是一个很好的模型系统，用于测试自发性癌症发展之前镉和锌对LH和睾丸激素及其他雄激素产生的影响。

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