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大鼠肝脏和骨骼肌中的抗氧化酶系统。硒缺乏、长期训练及急性运动的影响。

Antioxidant enzyme systems in rat liver and skeletal muscle. Influences of selenium deficiency, chronic training, and acute exercise.

作者信息

Ji L L, Stratman F W, Lardy H A

机构信息

Institute for Enzyme Research, University of Wisconsin, Madison 53705.

出版信息

Arch Biochem Biophys. 1988 May 15;263(1):150-60. doi: 10.1016/0003-9861(88)90623-6.

Abstract

The influences of selenium deficiency (Se-D), chronic training, and an acute bout of exercise on hepatic and skeletal muscle antioxidant enzymes, i.e., superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPX), as well as glutathione S-transferase (GST) and tissue lipid peroxidation, were investigated in post-weaning male Sprague-Dawley rats. Se-D per se depleted GPX in both liver and skeletal muscle but had no effect on SOD or catalase activity. One hour of treadmill running (20 m/min, 0% grade and 27 m/min, 15% grade for untrained and trained rats, respectively) significantly elevated hepatic catalase and cytosolic SOD activity; more prominent activations were found in the Se-D or untrained rats, whereas skeletal muscle antioxidant enzymes were little affected. Ten weeks of training (1 h/day, 5 days/week at 27 m/min, 15% grade) increased hepatic mitochondrial SOD by 23% (P less than 0.05) in Se-D rats. Both hepatic mitochondrial and cytosolic GPX were decreased by training whereas GPX was increased twofold in skeletal muscle mitochondria. Se-independent GPX was elevated by training only in the skeletal muscle mitochondria of Se-D rats. Lipid peroxidation (malondialdehyde formation) was increased by an acute bout of exercise in hepatic mitochondria of the untrained rats and in skeletal muscle mitochondria of the Se-D rats. These data indicate that antioxidant enzymes in liver and skeletal muscle are capable of adapting to selenium deficiency and exercise to minimize oxidative injury caused by free radicals.

摘要

研究了断奶后雄性斯普拉格-道利大鼠缺硒(Se-D)、长期训练和一次急性运动对肝脏和骨骼肌抗氧化酶,即超氧化物歧化酶(SOD)、过氧化氢酶和谷胱甘肽过氧化物酶(GPX),以及谷胱甘肽S-转移酶(GST)和组织脂质过氧化的影响。缺硒本身会使肝脏和骨骼肌中的GPX减少,但对SOD或过氧化氢酶活性没有影响。一小时的跑步机跑步(未训练和训练大鼠分别为20米/分钟、0%坡度和27米/分钟、15%坡度)显著提高了肝脏过氧化氢酶和胞质SOD活性;在缺硒或未训练的大鼠中发现了更显著的激活,而骨骼肌抗氧化酶受影响较小。十周的训练(每天1小时,每周5天,速度为27米/分钟,坡度为15%)使缺硒大鼠肝脏线粒体SOD增加了23%(P小于0.05)。训练使肝脏线粒体和胞质中的GPX均降低,而骨骼肌线粒体中的GPX增加了两倍。仅在缺硒大鼠的骨骼肌线粒体中,训练使不依赖硒的GPX升高。急性运动使未训练大鼠肝脏线粒体和缺硒大鼠骨骼肌线粒体中的脂质过氧化(丙二醛形成)增加。这些数据表明,肝脏和骨骼肌中的抗氧化酶能够适应缺硒和运动,以尽量减少自由基引起的氧化损伤。

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