OBJECTIVE: We investigated the effect of dietary magnesium (Mg) deficiency on the bioavailability and tissue distribution of selenium (Se). METHODS: Wistar rats were fed an Mg-deficient diet for 70 days (D). Selenium content in plasma, whole blood, skeletal muscle, heart, kidney and femoral bone was determined after 7, 35, 49 and 70 days on a Mg-deficient diet. RESULTS: The Mg-deficient diet significantly decreased Se absorption from week 7 until the end of the experimental period; this effect was accompanied by a significant decrease in Se balance. We found a direct linear correlation between Se absorption and retention (balance) (pair-fed controls r = 0.842, p < 0.001; Mg-deficient rats r = 0.959, p < 0.001), and between Se absorbed and plasma Se concentration (controls r = 0.527, p < 0.02; Mg-deficient rats r = 0.704, p < 0.001). In general there were no significant correlations between urinary Se and any other parameter. Tissue analyses showed that after 7 days, Mg deficiency reduced erythrocyte Se and significantly increased plasma and kidney Se. Heart Se was significantly increased only at the end of the study. We found no significant changes in skeletal muscle or bone Se at any time during the experimental period. CONCLUSION: Chronic Mg deficiency decreases Se absorption and retention and erythrocyte concentrations of this mineral, and increases Se in plasma, kidney and heart. Under our experimental conditions, absorption appears to play an important role in the regulation of the tissue distribution of Se.
OBJECTIVE: We investigated the effect of dietary magnesium (Mg) deficiency on the bioavailability and tissue distribution of selenium (Se). METHODS:Wistar rats were fed an Mg-deficient diet for 70 days (D). Selenium content in plasma, whole blood, skeletal muscle, heart, kidney and femoral bone was determined after 7, 35, 49 and 70 days on a Mg-deficient diet. RESULTS: The Mg-deficient diet significantly decreased Se absorption from week 7 until the end of the experimental period; this effect was accompanied by a significant decrease in Se balance. We found a direct linear correlation between Se absorption and retention (balance) (pair-fed controls r = 0.842, p < 0.001; Mg-deficient rats r = 0.959, p < 0.001), and between Se absorbed and plasma Se concentration (controls r = 0.527, p < 0.02; Mg-deficient rats r = 0.704, p < 0.001). In general there were no significant correlations between urinary Se and any other parameter. Tissue analyses showed that after 7 days, Mg deficiency reduced erythrocyte Se and significantly increased plasma and kidney Se. Heart Se was significantly increased only at the end of the study. We found no significant changes in skeletal muscle or bone Se at any time during the experimental period. CONCLUSION: Chronic Mg deficiency decreases Se absorption and retention and erythrocyte concentrations of this mineral, and increases Se in plasma, kidney and heart. Under our experimental conditions, absorption appears to play an important role in the regulation of the tissue distribution of Se.