Sagai M, Ichinose T
Division of Basic Medical Sciences, National Institute for Environmental Studies, Ibaraki, Japan.
Environ Health Perspect. 1987 Aug;73:179-89. doi: 10.1289/ehp.8773179.
This work was done to clarify the relation between the changes of lipid peroxidation and the activities of antioxidative protective enzymes in lungs of rats exposed acutely, subacutely, and chronically to nitrogen dioxide. It was confirmed that the activities of the antioxidative enzymes to protect cells from oxidative stress increased in an early phase, and then the activities decreased gradually. Lipid peroxides increased once in an early phase and then returned to the control level; thereafter, lipid peroxides increased gradually again. Lipid peroxidation as measured by ethane exhalation increased significantly with 0.04, 0.4, and 4 ppm nitrogen dioxide exposure for 9, 18, and 27 months, and a dose-response relationship was clearly observed. The temporal changes of lipid peroxidation varied inversely with that of the activities of antioxidative protective enzymes. From these results, it was suggested that the increments of antioxidative protective enzyme activities in an early phase were complementary effects to protect cells from damage by lipid peroxides which were increased by nitrogen dioxide exposure, and that the complementary effects are lost in later phases of life-span exposure. Finally, loss of such protective complementary effects might relate to some chronic diseases in lungs. Therefore, the temporal changes described above are important characteristics in chronic exposure of air pollutants.
本研究旨在阐明急性、亚急性和慢性暴露于二氧化氮的大鼠肺组织中脂质过氧化变化与抗氧化保护酶活性之间的关系。结果证实,保护细胞免受氧化应激的抗氧化酶活性在早期升高,随后逐渐降低。脂质过氧化物在早期曾一度增加,然后恢复到对照水平;此后,脂质过氧化物又逐渐增加。通过乙烷呼出量测定的脂质过氧化在暴露于0.04、0.4和4 ppm二氧化氮9、18和27个月时显著增加,且明显观察到剂量-反应关系。脂质过氧化的时间变化与抗氧化保护酶活性的变化呈相反趋势。从这些结果推测,早期抗氧化保护酶活性的增加是一种互补效应,以保护细胞免受因二氧化氮暴露而增加的脂质过氧化物的损伤,而这种互补效应在寿命暴露的后期会丧失。最后,这种保护性互补效应的丧失可能与肺部的一些慢性疾病有关。因此,上述时间变化是空气污染物慢性暴露的重要特征。