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糖尿病和饥饿大鼠不同组织中的抗氧化酶状态及脂质过氧化

Antioxidant enzyme status and lipid peroxidation in various tissues of diabetic and starved rats.

作者信息

Asayama K, Hayashibe H, Dobashi K, Niitsu T, Miyao A, Kato K

机构信息

Department of Pediatrics Yamanashi Medical College, Japan.

出版信息

Diabetes Res. 1989 Oct;12(2):85-91.

PMID:2561353
Abstract

The effect of short term (2-wk) diabetes induced by streptozotocin and starvation (1-wk) on antioxidant enzymes and lipid peroxidation in the liver, kidney and heart of rats was investigated. The activity of mitochondrial oxidative markers was increased in diabetic liver and kidney, while the activity in tissues of starved rats tended to be decreased. Immunoreactive manganese superoxide dismutase was increased only in diabetic liver and was unchanged or decreased in the rest of the tissues. Glutathione peroxidase activity was increased in tissues of diabetic but not starved rats. The changes in copper-zinc superoxide dismutase and catalase in diabetic rats were similar to those in starved rats. In both groups, copper-zinc superoxide dismutase was decreased in liver, while catalase activity was decreased in liver and kidney, and increased in heart. The lipid peroxide level was increased in diabetic kidney and in the heart of starved rats, and decreased in the rest of the tissues. Insulin treatment in diabetic rats and refeeding in starved rats restored most of the abnormalities toward normal. These results suggest that accelerated mitochondrial oxidative metabolism not accompanied by induction of manganes superoxide dismutase results in oxidative injury in the hypertrophied kidney at an early stage of diabetes and possibly contributes to the development of nephropathy. Peroxidative myocardial damage in starved rat appears to be mediated by a catabolic process.

摘要

研究了链脲佐菌素诱导的短期(2周)糖尿病和饥饿(1周)对大鼠肝脏、肾脏和心脏中抗氧化酶及脂质过氧化的影响。糖尿病大鼠肝脏和肾脏中线粒体氧化标志物的活性增加,而饥饿大鼠组织中的活性则有降低趋势。免疫反应性锰超氧化物歧化酶仅在糖尿病大鼠肝脏中增加,在其余组织中无变化或降低。谷胱甘肽过氧化物酶活性在糖尿病大鼠组织中增加,而在饥饿大鼠中未增加。糖尿病大鼠铜锌超氧化物歧化酶和过氧化氢酶的变化与饥饿大鼠相似。在两组中,肝脏中铜锌超氧化物歧化酶均降低,肝脏和肾脏中过氧化氢酶活性降低,心脏中过氧化氢酶活性增加。脂质过氧化物水平在糖尿病大鼠肾脏和饥饿大鼠心脏中升高,在其余组织中降低。糖尿病大鼠的胰岛素治疗和饥饿大鼠的再喂养使大多数异常恢复正常。这些结果表明,加速的线粒体氧化代谢未伴随锰超氧化物歧化酶的诱导,在糖尿病早期导致肥大肾脏的氧化损伤,并可能促进肾病的发展。饥饿大鼠的过氧化心肌损伤似乎由分解代谢过程介导。

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