Transport of cadmium and manganese in mammals

通过体内和体外系统研究了锰转运系统在镉积累和毒性中的作用。同时在培养基中添加Mn或Zn可抑制MT细胞中Cd的细胞积累，并呈剂量依赖性。同时，锰和锌对镉的细胞毒性具有剂量依赖性，表明对镉、锰和锌具有高亲和力的转运系统在镉进入细胞中起重要作用。Mn在老鼠,同时政府或公司与Cd显示显著降低肝毒性和睾丸出血引起的Cd。这些影响也观察到金属硫蛋白基因敲除小鼠,表明金属硫蛋白没有参与锰和钴的保护。然而,组织Cd浓度没有改变,通过合并施打Mn或公司与Cd。尽管保护作用的锰和钴Cd毒性不解释的变化组织积累的Cd,IL-6在Cd毒性保护中的新作用。这些数据表明，在哺乳动物的特定细胞系中，Mn参与了Cd的沉积和毒性，而不是所有细胞。细胞因子，特别是IL-6，在体内对锰和钴镉毒性的影响有待于进一步的研究。

The roles of Mn transport system on the accumulation and toxicity of Cd were studied using both in vitro and in vivo systems. Cellular accumulation of Cd in MT null cells was inhibited by simultaneous addition of Mn or Zn in the medium dose-dependently. In parallel, cytotoxicity of Cd was inhibited by Mn and Zn dose-dependently, suggesting that the transport system having high affinity for Cd, Mn and Zn plays an important role in Cd incorporation into cells. In mice, simultaneous administration of Mn or Co with Cd showed marked decreases in hepatotoxicity and testicular hemorrhage caused by Cd. These effects were also observed in metallothionein knockout mice, suggesting that metallothionein is not involved in the protection by Mn and Co. However, tissue Cd concentrations were not altered, by co-administration of Mn or Co with Cd. Although protective effects of Mn and Co on Cd toxicity were not explained by the change in tissue accumulation of Cd, a novel role of IL-6 in the protection against Cd toxicity was implicated. These data suggest that Mn is involved in the deposition and toxicity of Cd in specific cell lines but not all cells of mammals. Involvement of cytokine, especially IL-6, in in vivo effects of Mn and Co on Cd toxicity should be clarified in future studies.