Liver mitochondria from manganese-deficient and pallid mice: function and ultrastructure.

Oxidative phosphorylation was studied in isolated liver mitochondria from manganese-deficient mice and in those from a mutant strain, pallid. In mitochondria from manganese-deficient mice, ratios of adenosine triphosphate formed to oxygen consumed were normal, but oxygen uptake was reduced. Electron microscopy of these mitochondria revealed ultrastructural abnormalities including elongation and reorientation of cristae. No biochemical or structural abnormalities were found in mitochondria from pallid mice.

Teratogenic effects of magnesium deficiency in rats.

The effect of severe magnesium deficiency on plasma magnesium levels in pregnant and nonpregnant rats and on reproduction was investigated. Magnesium deficiency produced a rapid fall in plasma magnesium concentration, in both pregnant and nonpregnant rats. At term, all implantation sites of pregnant rats fed a diet severely deficient in magnesium showed total fetal resorption. When pregnant females were fed the magnesium deficient diet only between days 6 and 14 of gestation, there was a high incidence of resorptions and gross malformations were seen in full term fetuses. The results demonstrate the rapidity of the effects of severe magnesium deficiency in pregnant rats and indicate the importance of the element for embryonic development.

Magnesium, calcium and zinc levels of maternal and fetal tissues in magnesium deficient rats.

The interaction of magnesium with two other mineral elements, calcium and zinc, was studied in maternal tissues and fetuses of pregnant rats fed a magnesium deficient diet throughout gestation. Reduction in maternal femur magnesium and a trend for increased kidney calcium reflected the dietary magnesium deficiency. In fetuses, however, total magnesium content was reduced and , in addition, fetal zinc content was also lower than normal in the group most severly deficient in magnesium. The possible interpretation of this magnesium-zinc interaction is discussed.

Magnesium deficiency anemia in the rat fetus.

Magnesium-deficient fetuses exhibited malformations (44%), anemia, and edema. Maternal plasma magnesium levels at day 21 of pregnancy reflected the level of dietary magnesium (2.43 +/- 0.09 mg Mg/100 ml, control; 0.74 +/- 0.02 mg Mg/100 ml, deficient). Plasma magnesium levels of deficient fetuses showed similar decreases although all fetal magnesium values at term were hihger than maternal values from the same group (3.29 +/- 0.22 mg Mg/100 ml, control; 1.78 +/- 0.07 mg Mg/100 ml, deficient). Magnesium deficiency did not appear to affect the maternal blood parameters. However, when fetal blood was examined, all of the parameters measured were altered in magnesum-deficient fetuses (Table 2). No abnormalities in hemoglobin bands or plasma proteins were seen between any groups by electrophoresis. Measurement of total protein contents showed no differences between maternal blood protein contents, but total plasma protein from magnesium-deficient fetuses was significantly lower than controls (2.00 +/- 0.14 versus 2.62 +/- 0.13 g/100 ml), thus establishing a factor in fetal edema production. Morphologic data showed that in magnesium-deficient fetuses, fetal erythropoiesis was significantly greater in liver, adrenal glands, and spleen than in controls and that maturation was normoblastic. Stained and unstained peripheral blood smears of magnesium-deficient fetuses showed and obvious macrocytosis and at least 50% of the red cells stained abnormally, exhibiting pale areas. Erythrocytic morphology seen in fetal magnesium deficiency is consistent with inadequate filling of the cell by hemoglobin as suggested by Cohlan et al. (5), a probable cause of membrane collapse. The inadequate filling of magnesium-deficient red blood cells (RBC) with hemoglobin might be explained by a reduction in hemoglobin synthesis which is consistent with the reduced mean corpuscular hemoglobin (MCH) and MCH concentration (MCHC) of the deficient fetal red cells. The role of magnesium in protein synthesis is also compatible with a reduction in hemoglobin synthesis, yet may not completely explain the abnormalities and resultant shortened lifespan of the red cells.