Mustea I, Bara A, Petrescu I, Révész L
Br J Cancer Suppl. 1978 Jun;3:159-62.
Misonidazole increased oxygen consumption of Ehrlich ascites cells and reversed the blockage of oxidative phosphorylation induced by amytal and KCN. It alos increased oxygen consumption of mitochondria in the presence of alpha-ketoglutarate substrate, but decreased the respiratory control ratio. Cellular oxygen consumption decreased, but mitochondrial consumption was increased by metronidazole, and the respiratory control ratio was not affected by this substance. It was concluded that misonidazole influences respiration in a similar way to uncouplers, and the interaction site for both substances is at the NADH level. These respiratory effects can be of importance in altering radiation response in multicellular tissues.
灭滴灵增加了艾氏腹水癌细胞的耗氧量，并逆转了由异戊巴比妥和氰化钾诱导的氧化磷酸化阻断。在存在α-酮戊二酸底物的情况下，它也增加了线粒体的耗氧量，但降低了呼吸控制率。甲硝唑使细胞耗氧量降低，但线粒体耗氧量增加，且该物质不影响呼吸控制率。得出的结论是，灭滴灵对呼吸的影响方式与解偶联剂相似，这两种物质的相互作用位点在NADH水平。这些呼吸效应在改变多细胞组织的辐射反应方面可能具有重要意义。
