The effect of magnesium deficiency on oxidative phosphorylation.

The uncoupling of oxidative phosphorylation in mitochondrial preparations by thyroxine and its reversal are now well known (l-6). More recently we have shown that high levels of dietary magnesium completely prevent the uncoupling effect on heart mitochondria of thyroxine-fed animals, and partially overcome the growth inhibition caused by thyroxine. Thyroxine thus raises the magnesium requirement. The gross signs observed in the thyroxine-treated animals were in many respects similar to those seen in magnesium deficiency (6). These observations suggested that magnesium deficiency alone might produce a similar uncoupling of oxidative phosphorylation. The results of this present paper demonstrate that such is the case. We have also studied the effects of thyroxine injection. The mitochondria of cardiac tissue are much more sensitive to the effects of thyroxine administration and magnesium deficiency than are those of liver and kidney.