Sohn H O, Lim H B, Lee Y G, Lee D W, Kim Y T
Laboratory of Biochemistry, Korea Ginseng, Taejon.
Arch Toxicol. 1993;67(10):667-73. doi: 10.1007/BF01973689.
Effects of subchronic administration of antioxidants against pulmonary damage mediated by cigarette smoke were investigated in rats. Rats were continuously received ascorbic acid, N-acetylcysteine and ginseng extract together drinking water from day 25 after birth. After 30 days of antioxidant supplementation, rats were exposed to cigarette smoke generated from six cigarettes (11 mg tar) for 20 min per day throughout 30 days, and then several biochemical markers related to the redox status in vivo were analyzed in the respiratory system. The cigarette smoke induced mild histological changes in trachea and lungs. The activity of superoxide dismutase (SOD) in the lung was significantly increased, and catalase and glutathione peroxidase activities were increased less than SOD, but total sulfhydryl compounds (Total-SH) content was decreased by cigarette smoking. In spite of the increase in activities of antioxidant enzymes, the inhibitory capacity of lung preparations on in vitro lipid peroxidation using ox brain homogenates was decreased and the change in the capacity was not related to the changes of these intracellular enzymes activities, but with the content of Total-SH. On the other hand, the content of thiobarbituric acid reactive substances and the ratio of elastase to anti-protease in the lung homogenates were significantly increased. Supplementation of antioxidants, however, effectively attenuated all of such alterations induced by cigarette smoke. These results indicate that although cigarette smoking induces antioxidant enzymes in the lung as a self defense mechanism, it seems to be not sufficient to protect the pulmonary system, and that chronic antioxidant feeding could be effective to reduce pulmonary damage induced by free radicals.
研究了亚慢性给予抗氧化剂对香烟烟雾介导的大鼠肺损伤的影响。从出生后第25天起,大鼠持续饮用含有抗坏血酸、N-乙酰半胱氨酸和人参提取物的水。在补充抗氧化剂30天后,大鼠每天暴露于六支香烟(11毫克焦油)产生的香烟烟雾中,持续30天,每天20分钟,然后分析呼吸系统中与体内氧化还原状态相关的几种生化标志物。香烟烟雾引起气管和肺部轻微的组织学变化。肺中超氧化物歧化酶(SOD)的活性显著增加,过氧化氢酶和谷胱甘肽过氧化物酶的活性增加幅度小于SOD,但吸烟会降低总巯基化合物(Total-SH)的含量。尽管抗氧化酶活性增加,但使用牛脑匀浆时肺组织制剂对体外脂质过氧化的抑制能力却下降了,这种能力的变化与这些细胞内酶活性的变化无关,而是与Total-SH的含量有关。另一方面,肺匀浆中硫代巴比妥酸反应性物质的含量以及弹性蛋白酶与抗蛋白酶的比例显著增加。然而,补充抗氧化剂有效地减轻了香烟烟雾引起的所有这些改变。这些结果表明,虽然吸烟会诱导肺中的抗氧化酶作为一种自我防御机制,但似乎不足以保护肺系统,并且长期给予抗氧化剂可能有效地减少自由基引起的肺损伤。