Gümüşlü S, Bilmen S, Korgun D K, Yargiçoğlu P, Ağar A
Department of Biochemistry, Faculty of Medicine, Akdeniz University, 07070, Arapsuyu, Antalya, Turkey.
Free Radic Res. 2001 Jun;34(6):621-7. doi: 10.1080/10715760100300511.
Antioxidant defenses within the lung are pivotal in preventing damage from oxidative toxicants. There have also been several reports with conflicting results on the antioxidant system during aging. In this study, we attempted to investigate age-related alterations in both antioxidant enzyme activities and thiobarbituric acid-reactive substances (TBARS), a product of lipid peroxidation, in the whole lung of control and sulfur dioxide (SO2) exposed rats of different age groups (3-, 12-, and 24-months-old). Swiss-Albino Male rats were exposed to 10 ppm. SO2 1 hr/day, 7 days/week for 6 weeks. The antioxidant enzymes examined include Cu,Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione S-transferase (GST). A mixed pattern of age-associated alterations in antioxidant activities was observed. SOD, GSH-Px and GST activities were increased with age, but CAT activity was decreased. Lung SOD, GSH-Px and GST activities were also increased in response to SO2. The level of TBARS was increased with age. SO2 exposure stimulated lipid peroxide formation in the lung as indicated by an increase in the level of TBARS. These findings suggest that both aging and SO2 exposure may impose an oxidative stress to the body. We conclude that the increase in the activities of the antioxidant enzymes of the lung during aging, could be interpreted as a positive feedback mechanism in response to rising lipid peroxidation.
肺内的抗氧化防御机制对于预防氧化毒物造成的损伤至关重要。关于衰老过程中的抗氧化系统,也有几份结果相互矛盾的报告。在本研究中,我们试图调查不同年龄组(3个月、12个月和24个月大)的对照大鼠和二氧化硫(SO₂)暴露大鼠全肺中抗氧化酶活性和硫代巴比妥酸反应性物质(TBARS,脂质过氧化产物)与年龄相关的变化。将瑞士白化雄性大鼠暴露于10 ppm的SO₂中,每天1小时,每周7天,持续6周。检测的抗氧化酶包括铜锌超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)和谷胱甘肽S-转移酶(GST)。观察到抗氧化活性随年龄变化呈现混合模式。SOD、GSH-Px和GST活性随年龄增加,但CAT活性降低。肺组织中的SOD、GSH-Px和GST活性也因SO₂暴露而增加。TBARS水平随年龄增加。SO₂暴露可刺激肺内脂质过氧化物的形成,表现为TBARS水平升高。这些发现表明,衰老和SO₂暴露都可能给身体带来氧化应激。我们得出结论,衰老过程中肺组织抗氧化酶活性的增加,可以解释为对脂质过氧化增加的一种正反馈机制。