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年龄对小鼠长期吸入香烟烟雾后谷胱甘肽代谢改变的影响。

Effect of age on alteration of glutathione metabolism following chronic cigarette smoke inhalation in mice.

作者信息

Teramoto S, Uejima Y, Teramoto K, Ouchi Y, Fukuchi Y

机构信息

Department of Geriatrics, Faculty of Medicine, University of Tokyo, Japan.

出版信息

Lung. 1996;174(2):119-26. doi: 10.1007/BF00177705.

DOI:10.1007/BF00177705
PMID:8919434
Abstract

Cigarette smoke is the most common oxidant stress in daily life and may affect the antioxidant capacity in humans and animals. The antioxidant functions may play an important role in preventing age-related disorders. However, influences of chronic cigarette smoke on the antioxidant capacity of visceral organs have not been investigated in the age. Senescene-accelerated mice (SAM) are good models for studying physiologic and/or pathologic aging. A senescene-prone strain, SAMP2, shows characteristics of premature aging. The senescence-resistant strain, SAMR1, exhibits relatively normal aging. In this study we examined the effects of chronic cigarette smoke exposure on the glutathione (GSH) metabolism of visceral organs in the two strains of mice that were 6 and 18 months old. After a 4-week cigarette or air exposure, total GSH and oxidized GSH (GSSG) in the organs were examined. In the young (6-month-old) mice, exposure to cigarette smoke caused a significant decrease of GSH in liver, blood, and lung of SAMP2 but not in those of SAMR1. In the aged (18-month-old) mice reduced GSH with a marked increase of GSSG were found in liver of both strains of SAM following cigarette smoke exposure. The baseline values of GSH and the GSSG/GSH ratio after air exposure were slightly changed with age, and the values after exposure to cigarette smoke were changed markedly with advancing age. These results indicate that GSH metabolism may be impaired by chronic cigarette smoke exposure in mice and that aged mice are more susceptible to cigarette smoke than young mice.

摘要

香烟烟雾是日常生活中最常见的氧化应激源,可能会影响人和动物的抗氧化能力。抗氧化功能在预防与年龄相关的疾病中可能发挥重要作用。然而,在这个年龄段,慢性香烟烟雾对内脏器官抗氧化能力的影响尚未得到研究。衰老加速小鼠(SAM)是研究生理和/或病理衰老的良好模型。早衰易感品系SAMP2表现出早衰的特征。抗衰品系SAMR1表现出相对正常的衰老过程。在本研究中,我们检测了慢性香烟烟雾暴露对6个月和18个月大的这两种品系小鼠内脏器官谷胱甘肽(GSH)代谢的影响。在进行4周的香烟或空气暴露后,检测器官中的总GSH和氧化型GSH(GSSG)。在年轻(6个月大)小鼠中,暴露于香烟烟雾导致SAMP2的肝脏、血液和肺中的GSH显著降低,但SAMR1的这些器官中没有。在老年(18个月大)小鼠中,香烟烟雾暴露后,两种品系的SAM肝脏中均发现GSH降低且GSSG显著增加。空气暴露后的GSH基线值和GSSG/GSH比值随年龄略有变化,而香烟烟雾暴露后的这些值随年龄增长变化显著。这些结果表明,慢性香烟烟雾暴露可能会损害小鼠的GSH代谢,并且老年小鼠比年轻小鼠更容易受到香烟烟雾的影响。

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本文引用的文献

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