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缺血条件下对离体大鼠心脏中泛醌合成的抑制作用。

Inhibition of ubiquinone synthesis in isolated rat heart under an ischemic condition.

作者信息

Sugawara H, Yamamoto T, Shimizu S, Momose K

机构信息

Department of Pharmacology, School of Pharmaceutical Sciences, Showa University, Tokyo, Japan.

出版信息

Int J Biochem. 1990;22(5):477-80. doi: 10.1016/0020-711x(90)90260-a.

Abstract
  1. The biosynthesis of ubiquinone (UQ) in isolated rat heart under ischemic and hypoxic conditions was investigated. 2. Under ischemic perfusion, a greater amount of biosynthetic intermediates, 3-nonaprenyl and 3-decaprenyl-4-hydroxybenzoate (PPHBs) was accumulated and a smaller amount of UQ-9 and -10 was synthesized when compared with normal conditions. 3. The accumulation of PPHBs was observed without forming UQs during anaerobic perfusion. 4. Hydroxylation which is the following reaction of PPHBs for the biosynthesis of UQ in rat heart, was proceeded by the monooxygenase(s) depending upon the oxygen concentrations.
摘要
  1. 研究了离体大鼠心脏在缺血和缺氧条件下泛醌(UQ)的生物合成。2. 在缺血灌注下,与正常条件相比,生物合成中间体3-壬基癸烯基和3-癸基癸烯基-4-羟基苯甲酸酯(PPHBs)积累量更多,而UQ-9和-10的合成量更少。3. 在无氧灌注期间观察到PPHBs的积累且未形成泛醌。4. 在大鼠心脏中,PPHBs后续用于泛醌生物合成的羟基化反应由取决于氧浓度的单加氧酶进行。

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