Stacey N H, Klaassen C D
J Toxicol Environ Health. 1981 Jan;7(1):149-58. doi: 10.1080/15287398109529966.
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 degrees C with vehicle (saline); Cd (200 or 400 microM); or Cd plus Cr, Mn, Zn, Ni, Pb, Se, or Fe (200-1000 microM). 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 the thiobarbituric acid reactants, were assessed. Uptake of 109Cd 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 seen in vivo can 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.
镉（Cd）与其他金属离子之间的相互作用在营养和毒理学方面都很重要。由于镉对分离的肝细胞有毒性，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℃下与溶剂（生理盐水）、镉（200或400微摩尔）或镉加铬、锰、锌、镍、铅、硒或铁（200 - 1000微摩尔）一起孵育。通过肝细胞内钾离子和天冬氨酸转氨酶的流失来评估细胞损伤的证据。通过硫代巴比妥酸反应物的浓度来评估对脂质过氧化的影响。还对109镉的摄取以及其他金属离子与这种积累的相互作用进行了定量。铬、锰、锌、铅和铁持续降低了镉引起的细胞损伤。铬、锰和锌抑制了镉引起的脂质过氧化。除镍外，所有金属都使肝细胞积累的镉量增加。细胞毒性的降低与脂质过氧化的抑制或镉的摄取之间没有一致的关系。这些实验表明：（1）在体内观察到的某些金属的保护特性在细胞水平上可以得到证明；（2）一般来说，金属对镉诱导的细胞毒性的保护作用不是由于镉摄取或脂质过氧化的减少。
