Glutathione metabolism of the red cells effect of glutathione reductase deficiency on the stimulation of hexose monophosphate shunt under oxidative stress

Riboflavin deficiency results in diminished glutathione reductase activity of the red cells of human subjects and of rats. The effect of such glutathione reductase deficiency on the rate of hexose monophosphate shunt pathway metabolism has been studied by measuring the rate of ¹⁴CO₂ production of red cells subjected to oxidative stress, measuring the rate of regeneration of GSH from GSSG, and by estimating the steady-state levels of GSSG and the rate of transport of GSSG from glutathione reductase-deficient red cells. No difference was observed between the red cells of normal subjects, of riboflavin-deficient (glutathione reductase-deficient) subjects, and the red cells of glutathione reductase-deficient subjects treated with riboflavin in vivo or in vitro to correct the glutathione reductase deficiency. These studies indicate that, in the red cell, glutathione reductase does not play limiting role in the rate of metabolism in the hexose monophosphate pathway.