[Energy metabolic changes and nerve cell damage in rats exposed to multiple administration of large-dose insulin]

The brains of rats that had experienced 5-7 hypoglycemic comas on day 2 of the rehabilitative period after the last coma showed increases in the activity NAD-isocitrate dehydrogenase and in the catabolism of adenylonucleotides and decreases in the activities ofNADH dehydrogenase, mitochondrial NADP-isocitrate dehydrogenase, glucose-6-phosphate dehydrogenase, glutathione reductase, and superoxide dismutase, and no changes in the rate of glycolysis. Placing the brain slices in the hypoosmolar medium added by Fe2+ and ascorbate caused the higher yield oflactate dehydrogenase into the incubation medium. In this case, there was a significant elevation in the concentration ofmalonic dialdehyde in the brain slices from the experimental rats. The findings suggest that energy metabolic disturbances and activated lipid peroxidation are involved in the pathogenesis of postglycemic encephalopathy.