Interaction of metal ions with cadmium-induced cellular toxicity.
Interaction of metal ions with cadmium-induced cellular toxicity.
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金属离子与镉诱导的细胞毒性的相互作用。
DOI：
10.1080/15287398109529966
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Klaassen,CD
中科院分区：
文献类型：
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作者：
Stacey,NH;Klaassen,CD
镉与其他金属离子之间的相互作用从营养学和毒理学方面都是重要的。由于镉对离体肝细胞具有毒性，因此这些细胞可用于研究其他金属对镉诱导的细胞损伤的影响。将分离的肝细胞在37°C下与溶剂（生理盐水）; Cd（200或400 μM）;或Cd + Cr、Mn、Zn、Ni、Pb、Se或Fe（200-1000 μM）孵育。通过肝细胞内K+和天冬氨酸转氨酶的损失评估细胞损伤的证据。通过硫代巴比妥酸反应物浓度测定，评估了对脂质过氧化的影响。109镉的吸收和其他金属离子与这种积累的相互作用也进行了定量。由于镉的细胞损伤是一贯减少铬，锰，锌，铅，铁。铬、锰和锌可抑制镉引起的脂质过氧化反应。所有的金属，但镍产生的肝细胞积累的镉的量增加。细胞毒性的降低与脂质过氧化抑制或镉的吸收之间没有一致的关系。这些实验表明：（1）某些金属在体内的保护特性可以在细胞水平上得到证实;（2）金属对镉诱导的细胞毒性的保护作用一般不是由于镉吸收或脂质过氧化的减少。
Interactions between Cd and other metal ions are important from both nutritional and toxicological aspects. As Cd is toxic to isolated hepatocytes, these cells can be used to investigate the effects of other metals on Cd‐induced cellular injury. Isolated hepatocytes were incubated at 37°C with vehicle (saline); Cd (200 or 400 μM); or Cd plus Cr, Mn, Zn, Ni, Pb, Se, or Fe (200–1000 μM). Evidence of cellular injury was assessed by loss of Intracellular K+and aspartate aminotransferase from the hepatocytes. Effects on lipid peroxidation, as measured by concentration of thiobarbituric acid reactants, were assessed. Uptake of109Cd and interaction of the other metal ions with this accumulation were also quantitated. Cell injury due to Cd was consistently reduced by Cr, Mn, Zn, Pb, and Fe. Lipid peroxidation due to Cd was inhibited by Cr, Mn, and Zn. All the metals except Ni produced an increase in the amount of Cd accumulated by hepatocytes. There was no consistent relation between reduction of cellular toxicity and either inhibition of lipid peroxidation or uptake of Cd. These experiments show that (1) protective properties of some metals seenin vivocan be demonstrated at the cellular level and (2) protective effects of metals in general on Cd‐induced cellular toxicity are not due to a decrease in either Cd uptake or lipid peroxidation.