Gogvadze V, Kass G E, Boyer C S, Zhukova A, Kim Y, Orrenius S
Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino.
Biochem Biophys Res Commun. 1992 Jun 15;185(2):698-704. doi: 10.1016/0006-291x(92)91682-g.
The mechanism by which the free radical scavenger butylated hydroxytoluene (BHT) prevents cumene hydroperoxide-induced Ca2+ release from rat liver mitochondria was studied. In Ca(2+)-loaded mitochondria cumene hydroperoxide induced a rapid oxidation and subsequent hydrolysis of the pyridine nucleotides. In the presence of BHT, pyridine nucleotide oxidation by cumene hydroperoxide occurred but was reversible as hydrolysis was prevented by BHT. However, the addition of BHT directly to rat liver submitochondrial particles did not inhibit NAD+ hydrolysis or the formation of ADP-ribose from NAD+. Thus, whilst BHT prevented NAD+ hydrolysis in isolated mitochondria, this appeared not to be due to a direct effect of BHT on the NADase. It is concluded that the mechanism of action of BHT on cumene hydroperoxide-induced Ca2+ release from mitochondria involves the inhibition of pyridine nucleotide hydrolysis by an indirect mechanism rather than the radical scavenging properties of BHT.
研究了自由基清除剂丁基羟基甲苯（BHT）阻止氢过氧化异丙苯诱导的大鼠肝线粒体释放Ca2+的机制。在加载了Ca2+的线粒体中，氢过氧化异丙苯诱导吡啶核苷酸快速氧化并随后水解。在BHT存在的情况下，氢过氧化异丙苯引起的吡啶核苷酸氧化发生了，但由于BHT阻止了水解，所以是可逆的。然而，将BHT直接添加到大鼠肝亚线粒体颗粒中并不能抑制NAD+水解或由NAD+形成ADP-核糖。因此，虽然BHT在分离的线粒体中阻止了NAD+水解，但这似乎并非由于BHT对NAD酶的直接作用。得出的结论是，BHT对氢过氧化异丙苯诱导的线粒体Ca2+释放的作用机制涉及通过间接机制抑制吡啶核苷酸水解，而不是BHT的自由基清除特性。
