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酒精性肌病:补锌无效。

Alcoholic myopathy: lack of effect of zinc supplementation.

作者信息

Durán Castellón M C, González-Reimers E, López-Lirola A, Martín Olivera R, Santolaria-Fernández F, Galindo-Martín L, Abreu-González P, González-Hernández T

机构信息

Departamento de Medicina Interna, Hospital Universitario, Tenerife, Canary Islands, Spain.

出版信息

Food Chem Toxicol. 2005 Sep;43(9):1333-43. doi: 10.1016/j.fct.2005.03.006.

Abstract

A chronic form of myopathy has been described in alcoholics, characterized by atrophy of type II fibers, due both to reduced protein synthesis and increased protein breakdown. Increased production of reactive oxygen species could probably play a role in increased protein breakdown. In addition, treatment with zinc might be beneficial, since it acts as a cofactor of several enzymes involved in the synthesis of proteins and antioxidants as copper-zinc-superoxidedismutase (SOD) and selenium dependent glutathione peroxidase (GPX). Based on these facts, we analyze the relative and combined effects of ethanol, protein malnutrition and treatment with zinc, 227 mg/l in form of zinc sulphate, on muscle changes in 8 groups of adult Sprague-Dawley rats fed following the Lieber-de Carli model during 5 weeks. We also study the association between muscle histological changes and the activity of GPX, SOD and lipid peroxidation products (MDA), with hormones such as IGF-1, and with trace elements involved in antioxidant systems and/or in lipid peroxidation, such as selenium, copper, zinc, and iron. We found type IIa and IIb fiber atrophy in the alcoholic animals, especially in the low-protein fed ones. This effect was mainly due to protein deficiency. Zinc played no role at all. Muscle iron increased in ethanol, low protein fed rats, either with or without zinc, and was directly related with muscle MDA levels, which in turn were related with muscle atrophy, as was also found for serum IGF-1 levels. Ethanol was the main responsible for all these changes, although protein undernutrition also played an independent role in MDA levels. A positive interaction between ethanol and protein deficiency on serum IGF-1 was also detected. These results suggest that both protein deficiency and ethanol contribute to muscle atrophy observed in alcoholized rats; this atrophy is associated with increased lipid peroxidation and muscle iron overload. Treatment with zinc sulphate confers no benefit.

摘要

酒精性肌病的一种慢性形式已在酗酒者中被描述,其特征为Ⅱ型纤维萎缩,这是由于蛋白质合成减少和蛋白质分解增加所致。活性氧生成增加可能在蛋白质分解增加中起作用。此外,锌治疗可能有益,因为它作为几种参与蛋白质和抗氧化剂合成的酶的辅助因子,如铜锌超氧化物歧化酶(SOD)和硒依赖性谷胱甘肽过氧化物酶(GPX)。基于这些事实,我们分析了乙醇、蛋白质营养不良以及以硫酸锌形式存在的227毫克/升锌治疗对8组成年Sprague-Dawley大鼠肌肉变化的相对和联合作用,这些大鼠按照Lieber-de Carli模型喂养5周。我们还研究了肌肉组织学变化与GPX、SOD活性及脂质过氧化产物(MDA)之间的关联,以及与诸如IGF-1等激素,和与参与抗氧化系统和/或脂质过氧化的微量元素,如硒、铜、锌和铁之间的关联。我们发现酒精性动物中Ⅱa型和Ⅱb型纤维萎缩,尤其是在低蛋白喂养的动物中。这种效应主要归因于蛋白质缺乏。锌根本没有起到作用。在喂食乙醇、低蛋白的大鼠中,无论是否补充锌,肌肉铁含量都会增加,并且与肌肉MDA水平直接相关,而MDA水平又与肌肉萎缩相关,血清IGF-1水平也是如此。乙醇是所有这些变化的主要原因,尽管蛋白质营养不良在MDA水平方面也发挥了独立作用。还检测到乙醇和蛋白质缺乏对血清IGF-1有正向相互作用。这些结果表明,蛋白质缺乏和乙醇都导致了酒精化大鼠中观察到的肌肉萎缩;这种萎缩与脂质过氧化增加和肌肉铁过载有关。硫酸锌治疗并无益处。

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