Melatonin: the assumed latest cure- all drug

This study was carried out to evaluate the hormonal and some biochemical changes which might be caused by administration of melatonin [Mt] daily for five months to 36 albino rats of both sexes. Long-term administration of doses equivalent to human dose range of melatonin caused an increase in testosterone, a decrease in estradiol [E2] levels in males with no change in the levels of both hormones in females, an increase in follicular stimulating hormones [FSH] and luteinizing hormone [LH] and a decrease in prolactin [PRL] levels in both sexes. Serum glutamicoxalo-acetic transaminase [GOT], glutamic- pyruvic transaminase [GPT] and sorbitol dehydrogenase [SDH] showed a significant increase from the third month onwards, while serum urea and creatinine showed a significant increase only at the fifth month

Testicular lactate dehydrogenase and sorbitol dehydrogenase activity after intratesticular injection of dynorphin and morphine in male rats.

Testicular lactate dehydrogenase (LDH) and sorbitol dehydrogenase (SDH) activity were measured at 1 and 4 hr following intratesticular injection of morphine and dynorphin. Twenty five and 50 micrograms doses of morphine sulfate significantly reduced LDH activity at 1 hr after injection. Five and 25 micrograms doses of dynorphin reduced LDH activity both at 1 and 4 hr after treatment. Testicular SDH activity was increased by morphine at 1 hr followed by a decrease at 4 hr. Both doses of dynorphin significantly reduced SDH activity at 1 and 4 hr after treatment. These results indicate paracrine regulatory role for opioids in testicular metabolism.

Vitamins prevention of diabetic complication: effect of vitamins C and B6 on glycosylated hemoglobin and sorbitol dehydrogenase

The experiments were undertaken to assess the role of vitamin C [ascorbic acid] and vitamin B6 [pyridoxine] in relation to sorbitol dehydrogenase activity and glycosylated hemoglobin levels in sorbitol pathway linked neural and vascular dysfunction and nonenzymatic glycosylation in rats with alloxan induced diabetes. Vitamins C and B6 monotherapy were given orally to control and diabetic rats. After 30 days and 45 days of treatment, glycosylated hemoglobin levels were decreased significantly [p <0.05 to 0.001]. Sorbitol dehydrogenase activity in normal rats during vitamin C therapy were increased significantly [p <0.08 to 0.001] from 7 to 9 folds after 30 days and 45 days, respectively. In diabetic rats sorbitol dehydrogenase activity elevated about 2.5 folds. Vitamin B6 increased sorbitol dehydrogenase activity about 7 folds in normal and 3 to 2.5 folds after 30 days and 45 days, respectively, in diabetic rats. These observations together with other evidence, suggested the significant relationship between glycosylated hemoglobin, sorbitol dehydrogenase and intake of vitamin C and vitamin B6. The elevated sorbitol dehydrogenase activity associated with the previously reported sorbitol levels. These vitamins supplementation is effective in individuals with insulin-dependent diabetes mellitus [IDDM]. They may be potentially important in controlling glucose-induced nonenzymatic glycosylation of proteins and, therefore may be a preferable drugs for inhibiting glucose induced nonenzymatic glycosylation, neural and vascular dysfunction