PROPIONYL-L-CARNITINE - BIOCHEMICAL SIGNIFICANCE AND POSSIBLE ROLE IN CARDIAC METABOLISM

被引：59

作者：

SILIPRANDI, N ^{[1
]}

DILISA, F ^{[1
]}

MENABO, R ^{[1
]}

机构：

[1] CNR,CTR STUDIO FISIOL MITOCONDRIALE,I-35100 PADUA,ITALY

来源：

CARDIOVASCULAR DRUGS AND THERAPY | 1991年 / 5卷

关键词：

PROPIONYL-L-CARNITINE; CARDIAC METABOLISM; TRICARBOXYLIC ACID CYCLE; ISCHEMIA;

D O I：

10.1007/BF00128238

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Propionyl-CoA is formed principally during amino acid catabolism. It is then converted chiefly to succinate in a described three-step sequence. Free propionate is formed from propionyl-CoA to a very limited extent, but this anion can participate in a futile cycle of activation and hydrolysis, which can significantly deplete mitochondrial ATP. Free CoA and propionyl-CoA cannot enter or leave mitochondria, but propionyl groups are transferred between separate CoA pools by prior conversion to propionyl-L-carnitine. This reaction requires carnitine and carnitine acetyl transferase, an enzyme abundant in heart tissue. Propionyl-L-carnitine traverses both mitochondrial and cell membranes. Within the cell, this mobility helps to maintain the mitochondrial acyl-CoA/CoA ratio. When this ratio is increased, as in carnitine deficiency states, deleterious consequences ensue, which include deficient metabolism of fatty acids and urea synthesis. From outside the cell (in blood plasma), propionyl-L-carnitine can either be excreted in the urine or redistributed by entering other tissues. This process apparently occurs without prior hydrolysis and reformation. It is suggested that heart tissue utilizes such exogenous propionyl-L-carnitine to stimulate the tricarboxylic acid cycle (via succinate synthesis) and that this may explain its known protective effect against ischemia.

引用

页码：11 / 16

页数：6

共 20 条

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