大鼠肝脏和肺组织对马来酸二乙酯体内诱导的谷胱甘肽耗竭的脂质过氧化差异反应：抗氧化剂类黄酮（+）-氰定醇-3的作用。

Differential lipid peroxidative response of rat liver and lung tissues to glutathione depletion induced in vivo by diethyl maleate: effect of the antioxidant flavonoid (+)-cyanidanol-3.

作者信息

Videla L A, Valenzuela A, Fernández V, Kriz A

出版信息

Biochem Int. 1985 Mar;10(3):425-33.

Abstract

The administration of a single dose of diethyl maleate (DEM) to fed rats elicited a drastic decrease in the content of reduced glutathione (GSH) both in liver and lung tissues after 6 h of treatment. Cellular GSH depletion induced by DEM was accompanied by a marked increase in pulmonary lipid peroxidation which was completely abolished by (+)-cyanidanol-3, without changes in the liver. Superoxide dismutase (SOD) activity remained unchanged in both tissues in this situation. Hepatic and pulmonary GSH depletion induced by a second dose of DEM given 24 h later produced a further increase in lung lipid peroxidation and a diminution of pulmonary SOD activity. In this condition, hepatic lipid peroxidation and SOD activity were not altered. These results indicate that lung and liver tissues exhibit a different lipid peroxidative response to chemically-induced GSH depletion.

摘要

给喂食后的大鼠单次注射马来酸二乙酯（DEM），在治疗6小时后，肝脏和肺组织中还原型谷胱甘肽（GSH）的含量急剧下降。DEM诱导的细胞内GSH耗竭伴随着肺脂质过氧化的显著增加，而（+）-花青素-3可完全消除这种增加，肝脏则无变化。在这种情况下，两种组织中的超氧化物歧化酶（SOD）活性均保持不变。24小时后给予第二剂DEM诱导的肝脏和肺GSH耗竭，导致肺脂质过氧化进一步增加，肺SOD活性降低。在这种情况下，肝脏脂质过氧化和SOD活性未改变。这些结果表明，肺和肝脏组织对化学诱导的GSH耗竭表现出不同的脂质过氧化反应。