Muscle antioxidant status in chronic alcoholism
Muscle antioxidant status in chronic alcoholism
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DOI：
10.1097/00000374-200212000-00013
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发表时间：
2002-12-01
影响因子：
3.2
通讯作者：
Nicolás, JM
中科院分区：
文献类型：
--
作者：
Fernández-Solà, J;García, G;Nicolás, JM
背景：酒精摄入过量引起的慢性肌病是发达国家获得性骨骼肌病最常见的原因之一。其发病机制是多因素的，仅有部分阐明，抗氧化剂失衡被认为是影响其发展的一种II型糖解快抽动纤维亚群，对这种影响更敏感。方法：我们评估了41名慢性酒精中毒男性和12名年龄匹配的对照组肌肉样本的超氧化物歧化酶、谷胱甘肽过氧化物酶和谷胱甘肽还原酶的活性以及总的抗氧化状态能力。酒精性骨骼肌病根据标准组织学标准进行定义。我们评估了酒精摄入量、热量和蛋白质营养状况以及骨骼肌病的存在对这些抗氧化酶组织活性的影响。结果：与对照组相比，慢性酒精中毒患者骨骼肌中谷胱甘肽过氧化物酶活性降低16%，超氧化物歧化酶活性升高13%(p<；0.05)。结论：慢性酒精中毒患者肌肉抗氧化酶活性部分紊乱，但与肌病的存在、酒精摄入量及患者的营养状况无关。进一步的研究应评估本研究没有包括的其他方面，如肌肉部位抗氧化剂状态/氧化损伤的具体变化，特定纤维类型对酒精的敏感性，以及饮食或酒精饮料中抗氧化剂含量的类型和数量。
Background: Chronic myopathy due to excessive ethanol intake is one of the most frequent causes of acquired skeletal myopathy in developed countries. Its pathogenesis is multi-factorial, only partially clarified, and antioxidant imbalance has been suggested to influence its development, being a type II glucolytic, fast-twitch fiber subset more sensitive to this effect.Methods: We assessed superoxide dismutase, glutathione peroxidase, and glutathione reductase enzyme activities as well as the total antioxidant status capacity in muscle samples obtained from 41 chronic alcoholic males and 12 age-matched controls. Alcoholic skeletal myopathy was defined according to standard histologic criteria. We evaluated the influence of ethanol consumption, caloric and protein nutritional status, and the presence of skeletal myopathy with the tissue activities of these antioxidant enzymes.Results: Chronic alcoholics showed a 16% reduction in glutathione peroxidase and a 13% increase of superoxide dismutase in the skeletal muscle, compared with controls (p < 0.05, both). Muscle antioxidant changes in chronic alcoholics were not related to the presence of skeletal myopathy, parameters of alcohol consumption, or conventional nutritional parameters.Conclusions: Antioxidant muscle enzyme activities are partially disturbed in chronic alcoholism, although not related to the presence of myopathy, amount of ethanol consumed, or the nutritional status of the patients. Further studies should assess other aspects not included in the present study such as muscle site-specific changes in antioxidant status/oxidative damage, specific fiber-type sensitivity to alcohol, and type and quantity of antioxidant content of the diet or in the alcohol beverages.