Masini A, Ceccarelli-Stanzani D, Trenti T, Ventura E
Biochim Biophys Acta. 1984 Nov 28;802(2):253-8. doi: 10.1016/0304-4165(84)90169-7.
The respiratory parameters and the membrane potential of liver mitochondria from rats treated with either hexachlorobenzene, iron or hexachlorobenzene plus iron, to induce experimental porphyria, have been studied. Partial uncoupling of oxidative phosphorylation has been observed in mitochondria from hexachlorobenzene- and hexachlorobenzene plus iron-treated rats. Direct evidence has been presented that this uncoupling is due to the action of pentachlorophenol endogenously formed by metabolism of hexachlorobenzene. No irreversible damage of mitochondria membrane has been revealed under both these conditions. Normal oxidative phosphorylation has been found in mitochondria from rats treated with iron alone. In contrast, they presented an anomalous membrane potential, fully restored by oligomycin. A possible involvement of lipid peroxidation process, induced by iron, in causing these abnormalities has been suggested.
对用六氯苯、铁或六氯苯加铁处理以诱发实验性卟啉症的大鼠的呼吸参数和肝线粒体膜电位进行了研究。在六氯苯处理的大鼠和六氯苯加铁处理的大鼠的线粒体中观察到氧化磷酸化的部分解偶联。已有直接证据表明这种解偶联是由于六氯苯代谢内源性形成的五氯苯酚的作用。在这两种情况下均未发现线粒体膜有不可逆损伤。在用铁单独处理的大鼠的线粒体中发现氧化磷酸化正常。相反,它们呈现异常的膜电位,用寡霉素可使其完全恢复。有人提出铁诱导的脂质过氧化过程可能参与导致这些异常。