Calabrese V, Renis M, Calderone A, Russo A, Barcellona M L, Rizza V
Institute of Biochemistry, University of Catania, Italy.
Free Radic Biol Med. 1996;20(3):391-7. doi: 10.1016/0891-5849(95)02095-0.
It is generally accepted that lipid peroxides play an important role in the pathogenesis of ethanol-induced cellular injury and that free sulfhydryl groups are vital in cellular defense against endogenous or exogenous oxidants. It has been observed that oxidative stress induces the synthesis of the 70-kDa family of heat-shock proteins (HSPs). Furthermore, induction of HSPs represents an essential and highly conserved cellular response to a variety of stressful stimuli. In the present study, we measured the intracellular levels of HSP 70 proteins after administration of mild intoxicating and grossly intoxicating doses of ethanol to rats. Our results demonstrate that elevated doses of ethanol induce HSP in various brain areas, namely, cerebellum, hippocampus, and to a lesser extent, striatum or liver. Induction of HSP 70 protein was correlated with a marked depletion of intracellular bound thiols and a decrease in lipid peroxidation measured as MDA formation. These studies support the hypothesis that a redox mechanism may be involved in the heat-shock signal pathway.
一般认为，脂质过氧化物在乙醇诱导的细胞损伤发病机制中起重要作用，而游离巯基在细胞抵御内源性或外源性氧化剂方面至关重要。据观察，氧化应激可诱导70 kDa热休克蛋白（HSP）家族的合成。此外，HSP的诱导是细胞对各种应激刺激的一种基本且高度保守的反应。在本研究中，我们给大鼠施用轻度中毒剂量和严重中毒剂量的乙醇后，测量了细胞内HSP 70蛋白的水平。我们的结果表明，高剂量乙醇可在不同脑区诱导HSP，即小脑、海马体，在较小程度上还有纹状体或肝脏。HSP 70蛋白的诱导与细胞内结合巯基的显著消耗以及以丙二醛（MDA）形成来衡量的脂质过氧化作用的降低相关。这些研究支持了氧化还原机制可能参与热休克信号通路的假说。
