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.