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酒精性慢性骨骼肌病中肌肉降解的体外和体内评估。

Assessment in vitro and in vivo of muscle degradation in chronic skeletal muscle myopathy of alcoholism.

作者信息

Martin F C, Peters T J

机构信息

Division of Clinical Cell Biology, MRC Clinical Research Centre, Harrow, Middlesex, U.K.

出版信息

Clin Sci (Lond). 1985 Jun;68(6):693-700. doi: 10.1042/cs0680693.

Abstract
  1. Muscle protein breakdown in vivo has been studied by measurements of urinary 3-methyl-histidine/creatinine ratios. No differences were found between control subjects and chronic alcoholics either with or without proximal muscle wasting or cirrhosis. 2. Calculation of muscle turnover rates, with the correction of Afting et al. (1981, Biochemical Journal, 200, 449-452) for non-skeletal muscle contributions of 3-methylhistidine and creatinine, showed lower values for alcoholics compared with controls. 3. Tissue activities of a neutral protease, assayed by a novel, rapid and sensitive fluorimetric method, were similar in patients and controls. The activity did not vary with severity of atrophy or the presence of cirrhosis. 4. No evidence was therefore obtained to suggest that alcoholic myopathy is due to increased muscle breakdown.
摘要
  1. 通过测量尿中3-甲基组氨酸/肌酐比值来研究体内肌肉蛋白分解情况。在有或没有近端肌肉萎缩或肝硬化的对照组受试者和慢性酒精中毒者之间未发现差异。2. 根据阿夫廷等人(1981年,《生物化学杂志》,200卷,449 - 452页)对3-甲基组氨酸和肌酐非骨骼肌贡献的校正方法计算肌肉周转率,结果显示与对照组相比,酒精中毒者的值较低。3. 采用一种新颖、快速且灵敏的荧光测定法检测中性蛋白酶的组织活性,患者和对照组的活性相似。该活性不随萎缩严重程度或肝硬化的存在而变化。4. 因此,没有证据表明酒精性肌病是由于肌肉分解增加所致。

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