Comparable dose-response functions for the effects of glucose and fructose on memory.

A passive avoidance-to-active avoidance negative transfer paradigm was used to investigate in rats the effects of glucose and fructose on recently acquired memories. Immediate post-passive avoidance conditioning injections of glucose, fructose, or saline were followed 48 h later by active avoidance conditioning. Equimolar 10, 32, 100, and 2000 mg/kg sc doses of the two sugars significantly impaired acquisition of the reversal task, whereas 3.2 mg/kg doses of both sugars were without significant effect on subsequent performance and 320 mg/kg doses of both sugars significantly enhanced subsequent performance. The cubic trends for both dose-response functions were statistically significant and did not differ from each other. This is the first demonstration that glucose and fructose affect recently acquired memories in accord with comparable cubic dose-response functions, and that there are doses of both sugars that can enhance memory (as indicated by an increase in the number of trials required to reach criterion on the reversal task) and doses of both sugars that can impair memory (as indicated by a decrease in the number of trials required to reach criterion on the reversal task), compared to saline treatment. The similar cubic dose-response functions for glucose and fructose suggest that their mechanisms of action when they are injected peripherally are similar. In addition, because fructose does not readily pass the blood-brain barrier, the results suggest that these two monosaccharides may act through a common peripheral pathway.

Depressed erythrocyte glutathione reductase activity in sickle cell disease.

In a group of 27 sickle cell disease patients ranging in age from 2 yr 3 months to 43 yr, 13 (48%) were found to have depressed erythrocyte glutathione reductase activity suggesting riboflavin deficiency. Glutathione reductase activity coefficients did not correlate with riboflavin intakes which were calculated from 3-day diet records returned by 16 patients. Other causes of riboflavin deficiency including decreased absorption, altered metabolism, or increased excretion of the vitamin must be considered. The potential effect of depressed erythrocyte glutathione reductase activity in the sickle cell disease process is discussed.