Calabrese V, Testa G, Ravagna A, Bates T E, Stella A M
Biochemistry, Faculty of Medicine, Department of Chemistry, University of Catania, Viale Andrea Doria N degrees 6, Catania, 95100, Italy.
Biochem Biophys Res Commun. 2000 Mar 16;269(2):397-400. doi: 10.1006/bbrc.2000.2311.
Changes in glutathione (GSH) and glutathione disulfide (GSSG) levels and/or redox status have been suggested to mediate the induction of heat shock proteins (HSPs) that follows exposure to oxidizing agents such as ethanol. Here we report the effects of ethanol administration to rats at intracellular levels of GSH, GSSG, HSP70, and protein carbonyls in brain and liver. Following 7 days of ethanol administration, there was a significant decrease in GSH, a significant induction of HSP70, and a significant increase in protein carbonyls in all brain regions studied and in liver. In cortex, striatum, and hippocampus there was a significant correlation between (a) the decrease in GSH, (b) the increase in GSSG, and (c) the decrease in GSH/GSSG ratio and HSP70 levels induced in response to ethanol. These data support the hypothesis that a redox mechanism may be involved in the heat-shock signal pathway responsible for HSP70 induction in the brain.
谷胱甘肽（GSH）和谷胱甘肽二硫化物（GSSG）水平及/或氧化还原状态的变化被认为介导了热休克蛋白（HSPs）的诱导，这种诱导发生在暴露于如乙醇等氧化剂之后。在此，我们报告给大鼠施用乙醇对其脑和肝内GSH、GSSG、HSP70及蛋白质羰基水平的影响。在给予乙醇7天后，在所研究的所有脑区及肝脏中，GSH显著降低，HSP70显著诱导，蛋白质羰基显著增加。在皮质、纹状体和海马中，（a）GSH的降低、（b）GSSG的增加以及（c）GSH/GSSG比值的降低与乙醇诱导的HSP70水平之间存在显著相关性。这些数据支持了一种假说，即氧化还原机制可能参与了负责脑内HSP70诱导的热休克信号通路。
