Transmembrane Oxalate Flux Studies in Intact Erythrocytes of Magnesium-Deficient Rats

Defective membrane function has been implicated to be the primary lesion underlying the cellular disturbances in magnesium deficiency1. Hyperabsorption of oxalate in intestinal brush border membrane vesicles prepared from magnesium-deficient rats suggested that it might involve a defect in the cellular transport of oxalate2. To further test this hypothesis, transmembrane oxalate flux rate constant ‘K’3 was measured in intact erythrocytes from rats fed a magnesium deficient diet (70 mg/kg diet) and from pair-fed controls fed a magnesium-supplemented diet (722 mg/kg diet) for thirty days.