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[慢性弥漫性肝病患者呼出气体中的脂质过氧化标志物与微粒体氧化]

[Lipid peroxidation markers in the exhaled breath and microsomal oxidation in patients with chronic diffuse liver diseases].

作者信息

Loginov A S, Bendikov E A, Petrakov A V

出版信息

Ter Arkh. 1995;67(4):50-3.

PMID:7784977
Abstract

Low-molecular hydrocarbons (butan, pentan) from the exhaled air as lipid peroxidation (LPO) markers were quantified in patients with chronic diffuse liver diseases. The study was also made of microsomal oxidation enzymic activity by antipirin metabolism. The above parameters were followed up in the course of antioxidant treatment. As shown by total butan and pentan levels, LPO activity varied with the disease, being high in hepatic cirrhosis and primary biliary cirrhosis, but low in chronic active hepatitis and fat dystrophy. Increased levels of butan and pentan occurred in association with inhibited activity of P450-dependent monooxygenases. This was determined by antipirin biotransformation and confirmed by a strong inverse correlation between the amount of hydrocarbons and antipirin metabolites (4-hydroxy- and norantipirin) clearance. In the course of antioxidant therapy the most pronounced inhibiting action on formation of low-molecular hydrocarbons was distinctive of essenciale, pikamilon and copmplivit. Relevant efficacy of carsil was weaker. Similar regularity for these drugs takes place in relation to activation of microsomal oxidation.

摘要

对慢性弥漫性肝病患者呼出气体中的低分子碳氢化合物(丁烷、戊烷)作为脂质过氧化(LPO)标志物进行了定量分析。还通过安替匹林代谢对微粒体氧化酶活性进行了研究。在抗氧化治疗过程中对上述参数进行了跟踪。从丁烷和戊烷的总量来看,LPO活性因疾病而异,在肝硬化和原发性胆汁性肝硬化中较高,而在慢性活动性肝炎和脂肪营养不良中较低。丁烷和戊烷水平升高与P450依赖性单加氧酶活性受抑制有关。这通过安替匹林生物转化得以确定,并通过碳氢化合物量与安替匹林代谢物(4-羟基安替匹林和去甲安替匹林)清除率之间的强负相关得到证实。在抗氧化治疗过程中,对低分子碳氢化合物形成的最显著抑制作用在Essenciale、匹卡米隆和康普利维特中表现突出。卡西尔的相关疗效较弱。这些药物在微粒体氧化激活方面也有类似规律。

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