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

Abstract

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.