S-adenosyl-L-methionine co-administration prevents the ethanol-elicited dissociation of hepatic mitochondrial ribosomes in male rats.
S-adenosyl-L-methionine co-administration prevents the ethanol-elicited dissociation of hepatic mitochondrial ribosomes in male rats.
复制标题
S-腺苷-L-甲硫氨酸共同给药可防止雄性大鼠乙醇引起的肝线粒体核糖体解离。
DOI：
10.1111/j.1530-0277.2008.00803.x
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Cahill,Alan
中科院分区：
文献类型：
--
作者：
Sykora,Peter;Kharbanda,KusumK;Crumm,SaraE;Cahill,Alan
背景：长期乙醇喂养雄性大鼠可导致线粒体翻译降低，呼吸复合物水平和线粒体呼吸速率降低。此外，乙醇消耗已显示导致线粒体解离增加。S-腺苷-L-甲硫氨酸（SAM）是线粒体组装和随后稳定性所必需的，并在慢性乙醇喂养期间耗尽。方法：雄性Sprague-道利大鼠根据配对喂养设计，喂食营养充足的液体饮食，其中乙醇占36%的热量，持续28天。 对于某些动物，在饲料中补充200 mg/l SAM。 制备肝线粒体并分离线粒体核糖体。呼吸速率，ATP水平，呼吸复合物水平，和mitoribosome解离的程度determined.Results：28天的乙醇喂养被发现导致SAM含量降低，呼吸抑制，并增加mitoribosome解离。未检测到线粒体蛋白含量、呼吸复合物I、III和V水平、复合物I活性和ATP水平的变化。饮食中SAM的共同管理被发现，以防止乙醇诱导的SAM耗尽，呼吸减少和mitoribosome dissociation.Conclusions：总的来说，这些研究结果表明：（1），mitoribosome解离之前呼吸复合物抑郁症在酒精中毒的动物和（2），饮食补充SAM防止一些早期线粒体病变与慢性乙醇消耗。
Background:Chronic ethanol feeding to male rats has been shown to result in decreased mitochondrial translation, depressed respiratory complex levels and mitochondrial respiration rates. In addition, ethanol consumption has been shown to result in an increased dissociation of mitoribosomes. S‐adenosyl‐L‐methionine (SAM) is required for the assembly and subsequent stability of mitoribosomes and is depleted during chronic ethanol feeding. The ability of dietary SAM co‐administration to prevent these ethanol‐elicited lesions was investigated.Methods:Male Sprague‐Dawley rats were fed a nutritionally adequate liquid diet with ethanol comprising 36% of the calories according to a pair‐fed design for 28 days. For some animals, SAM was supplemented in the diet at 200 mg/l. Liver mitochondria were prepared and mitoribosomes isolated. Respiration rates, ATP levels, respiratory complex levels, and the extent of mitoribosome dissociation were determined.Results:Twenty‐eight days of ethanol feeding were found to result in decreased SAM content, depressed respiration, and increased mitoribosome dissociation. No changes in mitochondrial protein content; levels of respiratory complexes I, III, and V; complex I activities; and ATP levels were detected. Co‐administration of SAM in the diet was found to prevent ethanol‐induced SAM depletion, respiration decreases and mitoribosome dissociation.Conclusions:Taken together, these findings suggest (1) that mitoribosome dissociation precedes respiratory complex depressions in alcoholic animals and (2) that dietary supplementation of SAM prevents some of the early mitochondrial lesions associated with chronic ethanol consumption.