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[硫利达嗪视网膜病变的发病机制]

[Mechanism of the development of thioridazine retinopathy].

作者信息

Ivanina T A, Lebedeva M N, Sakina N L

出版信息

Biull Eksp Biol Med. 1988 Jan;105(1):22-5.

PMID:3337876
Abstract

Comparative electron microscopic, electrophysiological and biochemical studies of thioridazine influence on lipid peroxidation in vivo (rats, rabbits) and in vitro (model systems) were performed. It was shown that thioridazine retinopathy was not followed by an increase in lipid peroxidation and antioxidant (dibunol) failed to protect the retina against the destructive action of thioridazine. Moreover, thioridazine inhibited lipid peroxidation in model system.

摘要

进行了硫利达嗪对体内(大鼠、兔子)和体外(模型系统)脂质过氧化影响的比较电子显微镜、电生理和生化研究。结果表明,硫利达嗪性视网膜病变并未伴随脂质过氧化增加,抗氧化剂(二丁基羟基甲苯)未能保护视网膜免受硫利达嗪的破坏作用。此外,硫利达嗪在模型系统中抑制脂质过氧化。

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