Glutathione and related indices in rat lenses, liver and red cells during riboflavin deficiency and its correction.

Biochemical changes in lenses and at other sites in adult rats were investigated during the induction and correction of riboflavin deficiency. Riboflavin deficient (D), 1-day-repleted (R1), 2-days-repleted (R2), 16-days-repleted (R3), food-restricted, weight-matched controls (CFR) and ad libitum-fed controls (CAL) were compared. Activation coefficients of erythrocyte and lens glutathione reductase, which became abnormal in the deficient (D) animals, were corrected to varying extents in the repleted (R) groups. Hepatic flavin concentrations were lowered in the groups with raised glutathione. Inter-group differences in hepatic glutathione concentrations were not simply related to tissue flavin depletion or its reversal, but were complicated by changes in liver: body-weight ratios. Inter-group differences in lenticular glutathione levels were very small. In both liver and lens, sorbitol concentrations were lowest in group R3 and highest in groups D, R1 and R2. Lens ascorbate levels and the lens enzymes, aldose reductase, sorbitol dehydrogenase, glutathione peroxidase and superoxide dismutase, were not significantly affected by diet. Thiobarbituric acid-reactive substances were increased in riboflavin-deficient rat lenses but were lowered in riboflavin-deficient plasma samples. The results suggest overall that while riboflavin deficiency may affect certain biochemical indices, such as sorbitol and thiobarbituric-reactive substances, in the lens and other tissues, these changes are not the result of lowered glutathione levels. They also clearly demonstrate the importance of inanition as a confounding factor in the interpretation of changes resulting from riboflavin deficiency in experimental animals.