Maines M D, Kappas A
Clin Pharmacol Ther. 1977 Nov;22(5 Pt 2):780-90. doi: 10.1002/cpt1977225part2780.
The effects of metals as modifiers of the activity of microsomal drug-metabolizing enzymes were studied with the use of nickel, cobalt, and iron. These metals were found to impair cellular heme-dependent metabolism by affecting both the heme biosynthetic and heme degradative pathways, inhibiting the former and inducing the latter. As powerful cellular toxins, metals depress respiratory activity and indirectly reduce drug-detoxifying ability of cells. Metals also perturb cellular glutathione content and thus may alter the activity of glutathione-dependent enzymes. The toxicity of metals is cumulative depending on concentration and degree of cellular exposure to one or to several closely related metals. On the other hand, these metal effects on cellular heme metabolism could also have selective therapeutic application in circumstances in which it may be desirable to suppress heme synthesis in order to decrease drug biotransformation, i.e., when a certain drug metabolite is more toxic than the parent compound.
利用镍、钴和铁研究了金属作为微粒体药物代谢酶活性调节剂的作用。发现这些金属通过影响血红素生物合成和血红素降解途径来损害细胞血红素依赖性代谢,抑制前者并诱导后者。作为强大的细胞毒素,金属会抑制呼吸活性并间接降低细胞的药物解毒能力。金属还会扰乱细胞内谷胱甘肽含量,因此可能会改变谷胱甘肽依赖性酶的活性。金属的毒性具有累积性,这取决于其浓度以及细胞对一种或几种密切相关金属的暴露程度。另一方面,这些金属对细胞血红素代谢的影响在某些情况下也可能具有选择性治疗应用,即当希望抑制血红素合成以减少药物生物转化时(也就是说,当某种药物代谢物比母体化合物毒性更大时)。