, Volume 41, Issue 5, pp 197-202

Protective effect of calcium deficiency on the inflammatory response in magnesium-deficient rats

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Summary.

Background: Previous studies indicated that dietary Mg-deficiency in rats results in a marked pro-inflammatory effect. Since magnesium (Mg) frequently acts as a natural calcium (Ca) antagonist, the possibility exists that the pro-inflammatory effect of Mg-deficiency may be a consequence of a reduced extracellular Mg2+/Ca2+ antagonism. Aim of the study: Thus, the aim of the study was to assess whether dietary Ca-deficiency improves the abnormal inflammatory response of Mg-deficient rats. Materials and methods: Weaning male Wistar rats were randomly divided into 4 groups according to the dietary Mg and Ca as follows: Mg-adequate Ca-adequate (control), Mg-adequate Ca-deficient, Mg-deficient Ca-adequate, Mg-deficient Ca-deficient. Animals were fed the appropriate diets for 8 days. Results: Mg-deficient Ca-adequate rats as compared to controls displayed the usual decrease in plasma Mg, whereas the plasma Ca concentration was unaffected. The classical symptoms of inflammation including hyperemia, increased number of blood leukocytes and increased spleen weight were observed. In addition, these animals also showed an increase in heart lipid peroxidation and in plasma triglyceride concentration. In Mg-deficient rats, Ca-deficiency induced hypocalcemia and offered a significant protection against the pro-inflammatory effect of Mg-deficiency. This was evidenced by lower inflammation scores, prevention of leukocytosis and of spleen enlargement. The protective effects of Ca-deficiency on the inflammatory response in Mg-deficiency was accompanied by significant reduction in lipid peroxidation and by a normalization of plasma triglyceride concentration. Conclusion: All together, the results suggest that Ca is implicated in the inflammatory response of experimental Mg-deficiency and that oxidative stress and hypertriglyceridemia are the results of the acute phase response following Mg-deficiency in rats.

Received: 3 June 2002, Accepted: 14 August 2002
Correspondence to: Y. Rayssiguier