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肝脏缺血再灌注后大鼠肝脏内源性辅酶Q同系物、α-生育酚和谷胱甘肽水平的变化以及辅酶Q10预处理的影响

Changes in the levels of endogenous coenzyme Q homologs, alpha-tocopherol, and glutathione in rat liver after hepatic ischemia and reperfusion, and the effect of pretreatment with coenzyme Q10.

作者信息

Marubayashi S, Dohi K, Yamada K, Kawasaki T

出版信息

Biochim Biophys Acta. 1984 Jan 24;797(1):1-9.

PMID:6692004
Abstract

The present study was undertaken to determine whether hepatic ischemia and the subsequent reflow of blood had any effect on the levels of endogenous coenzyme Q homologs, alpha-tocopherol, and glutathione, and whether coenzyme Q10 (6 mg/kg of body weight) altered these levels. Ischemia of the rat liver for 90 min resulted in decreases of 19.1 and 19.6% of endogenous alpha-tocopherol and total glutathione (GSH + GSSG) without significant changes in the levels of endogenous total coenzyme Q homologs (oxidized and reduced). Restoration of the blood flow resulted in marked decreases in endogenous coenzyme Q homologs, alpha-tocopherol, and total glutathione in the control group. In coenzyme Q10-treated animals, however, there were no changes in the levels of endogenous total coenzyme Q9, alpha-tocopherol, or total glutathione as well as in the level of the enhanced total coenzyme Q10 during the reperfusion period. On the other hand, decreases in alpha-tocopherol and total glutathione during the period of ischemia remained unchanged. These results are compatible with the assumption that cellular damage caused by hepatic ischemia can be explained by free radical reaction processes during ischemia and especially, reperfusion and suggest that exogenous coenzyme Q10 functions as an antioxidant with endogenous coenzyme Q homologs, alpha-tocopherol, and glutathione in lipid peroxidation during reperfusion.

摘要

本研究旨在确定肝脏缺血及随后的血液再灌注对内源性辅酶Q同系物、α-生育酚和谷胱甘肽水平是否有影响,以及辅酶Q10(6mg/kg体重)是否会改变这些水平。大鼠肝脏缺血90分钟导致内源性α-生育酚和总谷胱甘肽(GSH + GSSG)分别降低19.1%和19.6%,而内源性总辅酶Q同系物(氧化型和还原型)水平无显著变化。恢复血流后,对照组内源性辅酶Q同系物、α-生育酚和总谷胱甘肽显著降低。然而,在辅酶Q10处理的动物中,再灌注期间内源性总辅酶Q9、α-生育酚或总谷胱甘肽水平以及增强的总辅酶Q10水平均无变化。另一方面,缺血期间α-生育酚和总谷胱甘肽的降低保持不变。这些结果与以下假设相符,即肝脏缺血引起的细胞损伤可以用缺血期间尤其是再灌注期间的自由基反应过程来解释,并表明外源性辅酶Q10在再灌注期间的脂质过氧化过程中与内源性辅酶Q同系物、α-生育酚和谷胱甘肽一起作为抗氧化剂发挥作用。

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