Effect of carbon tetrachloride on polyamine metabolism in rodent liver.
Effect of carbon tetrachloride on polyamine metabolism in rodent liver.
复制标题
四氯化碳对啮齿动物肝脏多胺代谢的影响。
DOI：
10.1016/0003-9861(82)90554-9
复制
发表时间：
1982
影响因子：
3.9
通讯作者：
Pegg,AE
中科院分区：
文献类型：
--
作者：
Pösö,H;Pegg,AE
肝毒性剂量的四氯化碳可使小鼠精胺/精胺N1-乙酰转移酶活性在6h内增加25倍，但对多胺氧化酶活性无明显影响。小鼠肝脏中乙酰化多胺的含量比检测下限增加了100多倍，达到每克组织0.6μ摩尔的N1-乙酰精胺和0.045μ摩尔的N1-乙酰精胺。腐胺水平也在6小时内增加了7倍，在24小时内增加了21倍。这些结果与四氯化碳引起的大鼠肝脏多胺的变化形成了对比。虽然肝毒素在该物种中产生了类似的亚精胺/亚精胺N1-乙酰转移酶的增加，但乙酰化多胺的增加要小得多，而且更短暂。N_1-乙酰亚精胺含量仅增加到0.066μ/g，未检出N_1-乙酰精胺。然而，大鼠的腐胺在6小时内增加了35倍，在16小时内增加了一倍，这些差异似乎是由于大鼠的多胺氧化酶活性比小鼠肝脏高得多，是小鼠肝脏的20倍。该酶将N1-乙酰精胺转化为亚精胺，并将N1-乙酰亚精胺降解为腐胺。在接触四氯化碳后，这两个物种的精胺含量都显著减少，但这种下降只有一部分可以归因于乙酰化的增加。
Administration of hepatotoxic doses of carbon tetrachloride to mice produced a 25-fold increase in spermidine/spermineN1-acetyltransferase activity within 6 h, but did not significantly change the activity of polyamine oxidase. The content of acetylated polyamines in the mouse liver was increased more than 100-fold from levels below the limit of detection to 0.6 μmol ofN1-acetylspermidine and 0.045 μmol ofN1-acetylspermine per gram of tissue. Putrescine levels also rose by 7-fold within 6 h and by 21-fold within 24 h. These results are in contrast to changes in hepatic polyamines brought about in the rat by carbon tetrachloride. Although the hepatotoxin produced a similar increase in spermidine/spermineN1-acetyltransferase in this species, the rise in acetylated polyamines was much smaller and more transient. The content ofN1-acetylspermidine was increased only to 0.066 μmol/g andN1-acetylspermine was not detected. However, in the rat putrescine increased 35-fold within 6 h and 64-fold by 16 h. These differences appear to be due to the much higher polyamine oxidase activity which was 20 times greater in the rat than in the mouse liver. This oxidase convertsN1-acetylspermine to spermidine and degradesN1-acetylspermidine to putrescine. Spermine content was significantly reduced in both species after exposure to carbon tetrachloride, but only part of this decline could be attributed to the increased acetylation.