镉对睾丸支持细胞的损伤机理研究

The rodent testes are generally more susceptible to cadmium(Cd)-induced toxicity than the liver. It is reported that the inability to induce the metal-detoxicating MT-protein, in response to Cd, might account for higher susceptibility of testes to Cd toxicity and carcinogenesis relative to liver. In order to clarify the molecular mechanism of Cd-induced toxicity in testes, Cd-induced metallothionein(MT) gene expression and MT protein accumulation under different time in testes and liver were compared. Our observations demonstrated that MT1 and MT2 mRNAs were expressed in testes under normal physiological conditions and there is no significant difference between testes and liver. our results have also shown that MT1 and MT2 mRNA both increased, but it did not translate into any higher protein in testes in response to Cd treatment. In summary, our observations clearly demonstrated that both MT mRNA and MT were constitutively expressed at high levels in isolated testicular individual cells and expression of MT mRNA isoforms are time- and cell-dependent. The inability to induce the metal-detoxicating MT-protein, in response to Cd, might account for higher susceptibility of testes to Cd toxicity and carcinogenesis relative to liver. It is important to clarify the molecular mechanism in Cd sensitivity and understand spermatogenic progression of testis.

本课题从损伤机理、保护机制及细胞功能改变三方面研究氏剂量镉对睾丸支持细胞可能损伤环节和机理。以镉在支持细胞内分布变化规律，结合离子钙的定位探讨其损伤机理；从金属硫蛋白表达与抗氧化酶活性改变关系研究睾丸MT保护作用；选取雄激素结合蛋白表达与吞噬功能来分析支持细胞功能改变。对揭示镉的睾丸毒性及破坏生精过程机理有重要意义。