The fumigant insecticide phosphine (PH3) is known to inhibit cytochrome c oxidase in vitro. Inhibition of the respiratory chain at this site has been shown to stimulate the generation of superoxide radicals (O2-), which dismutate to form hydrogen peroxide (H2O2). This study was performed in order to investigate the production of H2O2 by mitochondria isolated from granary weevil (Sitophilus granarius) and mouse liver on exposure to PH3. Other respiratory inhibitors, antimycin, myxothiazol, and rotenone were used with insect mitochondria. Hydrogen peroxide was measured spectrophotometrically using yeast cytochrome c peroxidase as an indicator. Insect and mouse liver mitochondria, utilizing endogenous substrate, both produced H2O2 after inhibition by PH3. Insect organelles released threefold more H2O2 than did mouse organelles, when exposed to PH3. Production of H2O2 by PH3-treated insect mitochondria was increased significantly on addition of the substrate alpha-glycerophosphate. Succinate did not enhance H2O2 production, however, indicating that the H2O2 did not result from the autoxidation of ubiquinone. NAD(+)-linked substrates, malate and pyruvate also had no effect on H2O2 production, suggesting that NADH-dehydrogenase was not the source of H2O2. Data obtained using antimycin and myxothiazol, both of which stimulated the release of H2O2 from insect mitochondria, lead to the conclusion that glycerophosphate dehydrogenase is a source of H2O2. The effect of combining PH3, antimycin, and myxothiazol on cytochrome spectra in insect mitochondria was also recorded. It was observed that PH3 reduces cytochrome c oxidase but none of the other cytochromes in the electron transport chain. There was no movement of electrons to cytochrome b when insect mitochondria are inhibited with PH3. The spectral data show that the inhibitors interact with the respiratory chain in a way that would allow the production of H2O2 from the sites proposed previously.

译文

:已知熏蒸杀虫剂膦(PH3)在体外可抑制细胞色素C氧化酶。已显示出在该部位抑制呼吸链会刺激超氧化物自由基(O2-)的生成,这些自由基会歧化形成过氧化氢(H2O2)。进行这项研究是为了研究暴露于PH3时从粮象鼻虫(Sitophilus granarius)和小鼠肝脏分离的线粒体产生H2O2。其他呼吸抑制剂,抗霉素,甲噻唑和鱼藤酮与昆虫线粒体一起使用。使用酵母细胞色素c过氧化物酶作为指示剂,通过分光光度法测量过氧化氢。昆虫和小鼠肝线粒体利用内源性底物,在被PH3抑制后均产生H2O2。当暴露于PH3时,昆虫细胞器释放的H2O2比小鼠细胞器释放的三倍。加入底物α-甘油磷酸后,PH3处理的昆虫线粒体产生的H2O2显着增加。琥珀酸酯并没有增加H2O2的产生,但是,这表明H2O2不是由泛醌的自氧化作用产生的。 NAD()连接的底物,苹果酸和丙酮酸也对H2O2的产生没有影响,这表明NADH脱氢酶不是H2O2的来源。使用抗霉素和甲噻唑获得的数据均刺激了昆虫线粒体释放H2O2,得出的结论是甘油磷酸脱氢酶是H2O2的来源。还记录了PH3,抗霉素和Mythothiazol组合对昆虫线粒体中细胞色素光谱的影响。观察到PH3会还原细胞色素c氧化酶,但在电子传输链中没有其他细胞色素。当昆虫线粒体被PH3抑制时,电子不会移动到细​​胞色素b。光谱数据表明,抑制剂与呼吸链相互作用的方式可以使先前提出的位点产生H2O2。

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