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酒精导致的老年大鼠肝脏初级抗氧化和谷胱甘肽家族酶的恶化可通过运动训练逆转。

Alcohol-induced deterioration in primary antioxidant and glutathione family enzymes reversed by exercise training in the liver of old rats.

机构信息

Department of Zoology, Sri Venkateswara University, Tirupati-517502, Andhra Pradesh, India.

出版信息

Alcohol. 2010 Sep;44(6):523-9. doi: 10.1016/j.alcohol.2010.07.004. Epub 2010 Aug 12.

Abstract

Chronic alcohol consumption causes severe hepatic oxidative damage, particularly to old subjects by decreasing various antioxidant enzymes. In this study, we test the hypothesis that exercise training can protect the aging liver against alcohol-induced oxidative damage. Two different age groups of Wistar albino rats (3 months young, n=24; 18 months old, n=24) were evenly divided into four groups: control (Con), exercise trained (Tr, 23 m/min 30 min/day, 5 days/week for 2 months), ethanol drinking/treated (Et, 2.0 g/kg b.w. orally), and exercise training plus ethanol drinking/treated (Tr+Et). We found significantly (P<.001) lowered hepatic antioxidant enzymes including superoxide dismutase, catalase, selenium (Se)-dependent glutathione peroxidase (Se-GSH-Px), Se-non-dependent glutathione peroxidase (non-Se-GSH-Px), glutathione reductase, and glutathione S-transferase activities in aged rats compared with young. Age-related decrease in antioxidant enzyme status was further exacerbated with ethanol drinking, which indicates liver in aged rats is more susceptible to oxidative damage because of decreased free radical scavenging system in aged/old ethanol-drinking rats. However, the decrease in liver antioxidant enzymes status with ethanol consumption was ameliorated by 2 months exercise training in old and young rats. These results demonstrate that age-associated decrease in hepatic free radical scavenging system exacerbated by ethanol drinking. For the first time, we found that this deterioration was significantly reversed by exercise training in aging liver, thus protects against alcohol-induced oxidative damage.

摘要

慢性酒精摄入会导致严重的肝氧化损伤,尤其是对老年人,会降低各种抗氧化酶。在这项研究中,我们检验了运动训练可以保护衰老的肝脏免受酒精引起的氧化损伤的假说。将两个不同年龄组的 Wistar 白化大鼠(3 个月龄的年轻组,n=24;18 个月龄的老年组,n=24)平均分为四组:对照组(Con)、运动训练组(Tr,23 m/min,每天 30 分钟,每周 5 天,持续 2 个月)、乙醇摄入/处理组(Et,2.0 g/kg b.w. 口服)和运动训练加乙醇摄入/处理组(Tr+Et)。我们发现,与年轻大鼠相比,老年大鼠的肝抗氧化酶活性显著(P<.001)降低,包括超氧化物歧化酶、过氧化氢酶、硒(Se)依赖性谷胱甘肽过氧化物酶(Se-GSH-Px)、非 Se 依赖性谷胱甘肽过氧化物酶(non-Se-GSH-Px)、谷胱甘肽还原酶和谷胱甘肽 S-转移酶。与年轻大鼠相比,年龄相关的抗氧化酶状态下降在乙醇摄入时进一步加剧,这表明由于衰老/老年乙醇摄入大鼠自由基清除系统的减少,肝脏更容易受到氧化损伤。然而,2 个月的运动训练可改善老年和年轻大鼠肝脏抗氧化酶状态的下降。这些结果表明,与年龄相关的肝自由基清除系统的下降加剧了乙醇摄入。这是首次发现,运动训练在衰老的肝脏中显著逆转了这种恶化,从而防止了酒精引起的氧化损伤。

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