| Manganese and magnesium interact to alter mitochondrial structure and function in swine and rats. In swine, feeding diets moderately high in Mn and low in Mg resulted in mortality with signs consistent with sudden cardiac death and necropsy indicated gross mineralization of heart tissue. A follow-up study using similar diets to the first study was conducted to elucidate the cause of deaths. Deaths occurred, and signs were similar to those observed previously. Heart muscle Mg was depressed in swine fed high Mn, low Mg diets; but not different when either adequate Mg or trace minerals were supplemented. In addition, high dietary Mn resulted in accumulation of Mn in liver and skeletal muscle, both metabolically active tissues rich with mitochondria. Electron microscopy of heart muscle revealed swollen and fragmented heart muscle mitochondria in swine fed high Mn, an effect that increased in severity with increased dietary Mn. Adequate dietary Mg eliminated the effect of swelling, even in swine fed high Mn. A rat model was used to study the potential mechanism of cardiomyopathy in swine. High dietary Mn reduced heart muscle O2 consumption; but had no effect on Ca-ATPase activity, antioxidant enzyme activity or cellular stress. Low Mg did not increase the retention or absorption of radiolabeled Mn. There was a strong Mn X Mg interaction where high Mn affected hematology in rats fed adequate Mg. The results of the research suggest that dietary Mn is toxic to mitochondria when combined with low Mg status through an undetermined mechanism. |
