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硫利达嗪治疗大鼠肾脏中木质素酸的脂质过氧化和氧化

Lipid peroxidation and oxidation of lignoceric acid in kidneys from thioridazine treated rats.

作者信息

Dhaunsi G S, Singh A K, Orak J, Singh I

机构信息

Department of Pediatrics and Pathology, Medical University of South Carolina, Charleston.

出版信息

J Exp Pathol. 1990;5(4):177-86.

PMID:2101135
Abstract

We have investigated lipid peroxidation and oxidation of lignoceric acid in response to oral thioridazine administration, to better understand the effects of phenothiazines, which are one of the more commonly used therapeutic agents. Measurements at different time intervals showed that levels of lipid peroxides in rat kidney were markedly decreased after thioridazine feeding, however, the oxidation of lignoceric acid was found to be elevated immediately after the start of thioridazine treatment. These biochemical changes were noted to be associated with mitochondrial proliferation and lipid accumulation in renal epithelial cells. The observed renal biochemical and morphological changes following thioridazine feeding return to the normal levels after two weeks of withdrawal of the drug. This study suggests that phenothiazines could be beneficial in reducing cellular injury by reducing the levels of lipid peroxides during pathological conditions like ischemia.

摘要

我们研究了口服硫利达嗪后脂质过氧化和木蜡酸氧化情况,以更好地了解吩噻嗪类药物的作用,这类药物是常用治疗药物之一。不同时间间隔的测量结果显示,喂食硫利达嗪后大鼠肾脏中的脂质过氧化物水平显著降低,然而,在硫利达嗪治疗开始后,木蜡酸的氧化立即升高。这些生化变化与肾上皮细胞中的线粒体增殖和脂质积累有关。喂食硫利达嗪后观察到的肾脏生化和形态学变化在停药两周后恢复到正常水平。这项研究表明,吩噻嗪类药物在缺血等病理状态下可能通过降低脂质过氧化物水平来减轻细胞损伤。

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