title: Alcoholic myopathy: lack of effect of zinc supplementation.
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.
authors.affiliation: Departamento de Medicina Interna, Hospital Universitario, Tenerife, Canary Islands, Spain.
authors.forename: M C
authors.initials: MC
authors.lastname: Durán Castellón
authors.forename: E
authors.initials: E
authors.lastname: González-Reimers
authors.forename: A
authors.initials: A
authors.lastname: López-Lirola
authors.forename: R
authors.initials: R
authors.lastname: Martín Olivera
authors.forename: F
authors.initials: F
authors.lastname: Santolaria-Fernández
authors.forename: L
authors.initials: L
authors.lastname: Galindo-Martín
authors.forename: P
authors.initials: P
authors.lastname: Abreu-González
authors.forename: T
authors.initials: T
authors.lastname: González-Hernández
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D002492:Central Nervous System Depressants / Q000633:toxicity*; D003300:Copper / Q000378:metabolism; D019587:Dietary Supplements; D000431:Ethanol / Q000633:toxicity*; D005979:Glutathione Peroxidase / Q000378:metabolism; D006728:Hormones / Q000097:blood; D007501:Iron / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D018485:Muscle Fibers, Skeletal / Q000473:pathology; D009124:Muscle Proteins / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology; D009135:Muscular Diseases / Q000139:chemically induced* / Q000473:pathology / Q000517:prevention & control*; D011488:Protein Deficiency / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012643:Selenium / Q000378:metabolism; D012709:Serum Albumin / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D015032:Zinc / Q000378:metabolism / Q000627:therapeutic use*
chemical_list: D000975:Antioxidants; D002492:Central Nervous System Depressants; D006728:Hormones; D009124:Muscle Proteins; D012709:Serum Albumin; D000431:Ethanol; D003300:Copper; D007501:Iron; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D012643:Selenium; D015032:Zinc