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对乙酰氨基酚诱导的发病机制中的氧化应激:(I)。肾损伤。

Oxidative stress in paracetamol-induced pathogenesis: (I). Renal damage.

作者信息

Abraham Premila

机构信息

Department of Biochemistry, Christian Medical College, Bagayam, Vellore 632 002, Tamil Nadu, India.

出版信息

Indian J Biochem Biophys. 2005 Feb;42(1):59-62.

PMID:23923583
Abstract

The effect of administration of paracetamol (1 g/kg body wt) on oxidative damage to proteins and lipids in the kidney was studied at various time intervals in adult male Wistar rats. Iindicators of oxidative stress, such as protein thiol, protein carbonyl content and lipid peroxide levels were assayed along with thiol-dependent enzyme activities, glutamine synthase and glyceraldehyde-3-phosphate dehydrogenase. Paracetamol-induced renal damage after 4 hr of administration was evidenced by elevation in plasma creatinine levels and the presence of acute tubular necrosis on histological examination of the kidney. No significant change in any other parameters was observed, except for decreased glutathione level. An increase in lipid peroxide level was observed at 24 hr after treatment. The results suggest that oxidative stress may not play a causative role, but contribute to the pathogenesis of paracetamol-induced renal damage.

摘要

在成年雄性Wistar大鼠的不同时间间隔,研究了给予对乙酰氨基酚(1克/千克体重)对肾脏中蛋白质和脂质氧化损伤的影响。测定了氧化应激指标,如蛋白质硫醇、蛋白质羰基含量和脂质过氧化物水平,以及硫醇依赖性酶活性、谷氨酰胺合成酶和甘油醛-3-磷酸脱氢酶。给药4小时后,对乙酰氨基酚诱导的肾损伤表现为血浆肌酐水平升高以及肾脏组织学检查发现急性肾小管坏死。除谷胱甘肽水平降低外,未观察到其他任何参数有显著变化。治疗后24小时观察到脂质过氧化物水平升高。结果表明,氧化应激可能不是对乙酰氨基酚诱导肾损伤的致病因素,但对其发病机制有影响。

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