Metabolic alterations produced in the liver by chronic ethanol administration. Comparison between the effects produced by ethanol and by thyroid hormones.

Metabolic alterations produced in the liver by chronic ethanol administration. Comparison between the effects produced by ethanol and by thyroid hormones.
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长期服用乙醇会导致肝脏代谢改变。

DOI:
10.1042/bj1340523
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发表时间:
1973
期刊:
The Biochemical journal
影响因子:
--
通讯作者:
J. Bernstein
J. Bernstein
中科院分区:
--
文献类型:
--
作者:
Y. Israel;L. Videla;A. Macdonald;J. Bernstein

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被引文献

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1.用甲状腺素处理的大鼠的肝切片显示O(2)消耗率增加。哇巴因可消除额外消耗,但不能消除基础呼吸。2.二硝基苯酚不能有效地增加甲状腺素处理动物肝切片的O(2)消耗率,但其有效性可以在哇巴因的存在下恢复。3. (Na(甲状腺素可使(+)+K(+))刺激的肝腺苷三磷酸酶活性升高。总Mg(2+)刺激的腺苷三磷酸酶活性无变化。4.线粒体α-甘油磷酸脱氢酶和微粒体NADPH氧化酶活性增加甲状腺素和慢性乙醇处理。5.长期用乙醇处理的动物的肝片合成尿素的速率增加。6.在长期使用乙醇处理的动物肝脏中,线粒体大小(截面积)显著增加。7.急性给予乙醇4和6 g/kg,可显著增加肝脏对~(131)I标记甲状腺素的摄取。8.本报告的工作,沿着其他研究者的结果,表明长期服用乙醇和甲状腺激素对肝脏产生的影响有显著的相似性。
1. Liver slices from rats treated with thyroxine show an increased rate of O(2) consumption. The extra consumption, but not the basal respiration, can be abolished by ouabain. 2. Dinitrophenol is not effective in increasing the rate of O(2) consumption of liver slices from thyroxine-treated animals but its effectiveness can be recovered in the presence of ouabain. 3. (Na(+)+K(+))-stimulated adenosine triphosphatase activity of liver was increased by administration of thyroxine in vivo. No changes were found in total Mg(2+)-stimulated adenosine triphosphatase activity. 4. Mitochondrial alpha-glycerophosphate dehydrogenase and microsomal NADPH oxidase activity were increased by both thyroxine and chronic ethanol treatment. 5. Liver slices from animals chronically treated with ethanol synthesize urea at an increased rate. 6. Mitochondrial size (section area) is markedly increased in the liver of animals chronically treated with ethanol. 7. Acute administration of ethanol in doses of 4 and 6g/kg significantly increases the uptake of (131)I-labelled thyroxine by the liver. 8. Work reported here, along with results from other investigators, indicates marked similarities between the effects produced in the liver by chronic administration of ethanol and by thyroid hormones.