ABSTRACT
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
Subject(s)
Animals, Laboratory , Rats , Testosterone/biosynthesis , Estradiol , /biosynthesis , Luteinizing Hormone/biosynthesis , Prolactin/drug effects , Aspartate Aminotransferases/drug effects , Alanine Transaminase/drug effects , L-Iditol 2-Dehydrogenase/drug effects , Creatine/blood , Urea/bloodABSTRACT
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.
Subject(s)
Analgesics, Opioid/pharmacology , Animals , Dynorphins/pharmacology , L-Iditol 2-Dehydrogenase/drug effects , L-Lactate Dehydrogenase/drug effects , Male , Microinjections , Morphine/pharmacology , Rats , Rats, Wistar , Testis/drug effectsABSTRACT
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