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心脏过氧化物酶体酶与饥饿

Cardiac peroxisomal enzymes and starvation.

作者信息

Crescimanno M, Armata M G, Rausa L, Gueli M C, Nicotra C, D'Alessandro N

机构信息

Istituto di Farmacologia e Sezione Autonoma di Oncologia Clinica, Palermo, Italy.

出版信息

Free Radic Res Commun. 1989;7(2):67-72. doi: 10.3109/10715768909087925.

Abstract

In mice subjected to 3-day periods of food deprivation an increase in plasma free fatty acids occurred together with a rise in the cardiac content of fatty acyl CoA-oxidase (+ 15.2%) and catalase (+ 136.2%) activities. Stimulation of hydrogen peroxide production by the heart was found after 30 hours of fasting and this phenomenon was almost completely eliminated by 6 hours of refeeding. These data suggest that high myocardial loads of free fatty acids involve the peroxisomal enzymes in the beta-oxidation process. The resulting increase in hydrogen peroxide production could be partly responsible for the myocardial injury caused by starvation.

摘要

在经历3天禁食期的小鼠中,血浆游离脂肪酸增加,同时心脏中脂肪酰基辅酶A氧化酶活性升高(+15.2%),过氧化氢酶活性升高(+136.2%)。禁食30小时后发现心脏产生过氧化氢增加,再喂食6小时后这种现象几乎完全消除。这些数据表明,心肌中高负荷的游离脂肪酸在β-氧化过程中涉及过氧化物酶体酶。由此导致的过氧化氢产生增加可能部分导致饥饿引起的心肌损伤。

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