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Dietary Magnesium Deficiency in Rats Enhances Free Radical Production in Skeletal Muscle^1,2,

INRA, Laboratoire des Maladies Métaboliques, 63122 Saint Genès Champanelle, France ^* CHRU, Hôtel-Dieu, Laboratoire de Biochimie, 63000 Clermont-Ferrand, France

Recent studies suggest that free radicals may be involved in tissue injuries induced by magnesium deficiency. The aim of the present study was to assess the effect of magnesium deficiency on free radical production of skeletal muscle tissue. Male Wistar rats were pair-fed from weaning for 12 d either control or Mg-deficient diets containing 960 or 40 mg magnesium/kg diet, respectively. In the Mg-deficient rats, hypomagnesemia was accompanied by significantly lower magnesium and greater calcium concentrations in skeletal muscle tissue. Electron microscopy of skeletal muscle tissue revealed ultrastructural changes, including swelling mitochondria and disorganization of the sar-coplasmic reticulum network. Using the spin-trapping technique, we showed that significantly more hydroxyl radicals were generated in muscle homogenates of Mg-deficient rats. Moreover, the amount of spin trap adducts was increased in the presence of exogenous iron in both groups. In agreement with these observations, a greater concentration of thiobarbituric acid-reactive substances and a lower concentration of thiol groups were found in skeletal muscle of the Mg-deficient group compared with controls. These results strongly support the hypothesis that free radical-mediated injury could contribute to skeletal muscle lesions resulting from magnesium deficiency.

KEY WORDS: • magnesium deficiency • skeletal muscle • spin trapping • peroxidation • rats

¹ Supported in part by funds from the Association Française contre les Myopathies (AFM, Evry, France) and the groupe DANONE, France.

² The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

³ To whom correspondence should be addressed.

Manuscript received 28 June 1994. Revision accepted 14 November 1994.

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