Yoshino K, Sano M, Hagiwara M, Fujita M, Tomita I
Laboratory of Health Science, School of Pharmaceutical Sciences, University of Shizuoka, Japan.
Biol Pharm Bull. 1993 Jan;16(1):84-6. doi: 10.1248/bpb.16.84.
Effects of lipid peroxide breakdown products, (E)-4-hydroxy-2-nonenal (4-HN) and n-hexanal, on mouse lung lesion were examined. When 4-HN was injected i.v., the plasma level of 4-HN increased just after the injection and then decreased immediately. The amounts of 4-HN increased in the liver and lung were ca. 0.085 and 0.43% to the dose administered, respectively, 5 min after the injection. Reduced glutathione (GSH) content and both GSH peroxidase (GSH-Px) and GSH reductase (GSSGR) activities in the lung were decreased significantly by 4-HN treatment. On the other hand, in the case of i.v. injection of n-hexanal into mice, the amount of n-hexanal detected in the lung was 5.0% to that of 4-HN, and no effect on the activities of GSH-Px and GSSGR and the content of GSH was observed. These results suggest that 4-HN generated from lipid peroxides would be transferred into the lung and cause the lung lesion through the inhibition of GSH-dependent antioxidative defense systems.
研究了脂质过氧化物分解产物（E）-4-羟基-2-壬烯醛（4-HN）和正己醛对小鼠肺部病变的影响。静脉注射4-HN后，注射后血浆中4-HN水平立即升高，随后迅速下降。注射后5分钟，肝脏和肺中4-HN的含量分别约为给药剂量的0.085%和0.43%。4-HN处理显著降低了肺中还原型谷胱甘肽（GSH）含量以及谷胱甘肽过氧化物酶（GSH-Px）和谷胱甘肽还原酶（GSSGR）的活性。另一方面，给小鼠静脉注射正己醛时，肺中检测到的正己醛量为4-HN的5.0%，未观察到对GSH-Px和GSSGR活性以及GSH含量的影响。这些结果表明，脂质过氧化物产生的4-HN会转移到肺中，并通过抑制GSH依赖的抗氧化防御系统导致肺部病变。
