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通过给予精氨酸降低大鼠海马体中的能量代谢。

Reduction of energy metabolism in rat hippocampus by arginine administration.

作者信息

Delwing Débora, Tagliari Bárbara, Streck Emílio Luiz, Wannamacher Clovis Milton Duval, Wajner Moacir, Wyse Angela Terezinha de Souza

机构信息

Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 2600-Anexo, CEP 90035-003, RS, Porto Alegre, Brazil.

出版信息

Brain Res. 2003 Sep 5;983(1-2):58-63. doi: 10.1016/s0006-8993(03)03029-4.

Abstract

Hyperargininemia is an inherited metabolic disease biochemically characterized by tissue accumulation of arginine. Mental retardation and other neurological features are common symptoms in hyperargininemic patients. Considering that the underlying mechanisms of brain damage in this disease are poorly established, in this work we investigated the effect of arginine administration to adult Wistar rats on some parameters of energy metabolism (CO(2) production, glucose uptake, lactate release and the activities of succinate dehydrogenase, complexes II and IV of the respiratory chain) in rat hippocampus. The action of L-NAME, an inhibitor of oxide nitric oxide synthase, on the effects produced by arginine was also tested. Sixty-day-old rats were treated with a single intraperitoneal injection of saline (group I, control), arginine (0.8 g/kg) (group II) or arginine (0.8 g/kg) plus L-NAME (2 mg/kg) (group III) and were killed 1 h later. Results showed that arginine administration significantly increased lactate release and diminished CO(2) production, glucose uptake, succinate dehydrogenase and complex II activities. In contrast, complex IV (cytochrome c oxidase) activity was not changed by this amino acid. Furthermore, simultaneous injection of L-NAME prevented some of these effects, except CO(2) production and lactate release. The present data indicate that in vivo arginine administration impairs some parameters of energy metabolism in hippocampus of rats probably through NO formation.

摘要

高精氨酸血症是一种遗传性代谢疾病,其生化特征为精氨酸在组织中蓄积。智力发育迟缓及其他神经学特征是高精氨酸血症患者的常见症状。鉴于该疾病脑损伤的潜在机制尚不明确,在本研究中,我们探究了给成年Wistar大鼠注射精氨酸对大鼠海马体能量代谢的一些参数(二氧化碳生成、葡萄糖摄取、乳酸释放以及琥珀酸脱氢酶活性、呼吸链复合物II和IV)的影响。我们还测试了一氧化氮合酶抑制剂L-NAME对精氨酸所产生效应的作用。给60日龄大鼠单次腹腔注射生理盐水(I组,对照组)、精氨酸(0.8 g/kg)(II组)或精氨酸(0.8 g/kg)加L-NAME(2 mg/kg)(III组),1小时后处死大鼠。结果显示,注射精氨酸显著增加了乳酸释放,减少了二氧化碳生成、葡萄糖摄取、琥珀酸脱氢酶及复合物II的活性。相比之下,该氨基酸并未改变复合物IV(细胞色素c氧化酶)的活性。此外,同时注射L-NAME可预防其中一些效应,但二氧化碳生成和乳酸释放除外。目前的数据表明,体内注射精氨酸可能通过一氧化氮的形成损害大鼠海马体的一些能量代谢参数。

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