普鲁卡因胺治疗的大鼠抗氧化活性增加。

Increase in antioxidant activity in procainamide-treated rats.

作者信息

Magner-Wróbel K, Toborek M, Drózdz M, Danch A

机构信息

Department of Biochemistry and Chemistry, Silesian Medical Academy, Poland.

出版信息

Pharmacol Toxicol. 1993 Feb;72(2):94-7. doi: 10.1111/j.1600-0773.1993.tb00297.x.

DOI:10.1111/j.1600-0773.1993.tb00297.x

PMID:8474970

Abstract

Recent studies suggest that in vivo procainamide oxidation underlies induction of autoimmunity by this drug. Since drug metabolism may be accompanied by generation of reactive oxygen species, plasma and liver thiobarbituric acid reacting substances (TBARS), activity of erythrocyte and liver superoxide dismutase, catalase, selenium-dependent glutathione peroxidase (Se-GPX), and plasma antioxidant activity in procainamide treated rats were evaluated. Procainamide administration increased liver lipid peroxide levels, intensified the activity of liver catalase and erythrocyte superoxide dismutase, as well as plasma antioxidant activity. The remaining biochemical parameters in the treated rats were within control values, except for the decreased erythrocyte catalase activity. We conclude, that the increased activity of free radicals observed in the treated rats could contribute to the development of procainamide induced side effects.

摘要

近期研究表明，体内普鲁卡因胺氧化是该药物诱发自身免疫的基础。由于药物代谢可能伴随着活性氧的产生，因此对普鲁卡因胺处理的大鼠的血浆和肝脏硫代巴比妥酸反应物质（TBARS）、红细胞和肝脏超氧化物歧化酶、过氧化氢酶、硒依赖性谷胱甘肽过氧化物酶（Se-GPX）的活性以及血浆抗氧化活性进行了评估。给予普鲁卡因胺会增加肝脏脂质过氧化物水平，增强肝脏过氧化氢酶和红细胞超氧化物歧化酶的活性以及血浆抗氧化活性。除红细胞过氧化氢酶活性降低外，处理大鼠的其余生化参数均在对照值范围内。我们得出结论，在处理的大鼠中观察到的自由基活性增加可能导致普鲁卡因胺诱发的副作用的发生。