Stress-induced increase in urinary isatin excretion in rats: reversal by both dexamethasone and alpha-methyl-P-tyrosine.
The effects of acute food deprivation and acute cold exposure on 24-hr urinary isatin excretion in rats and a mechanism responsible for changes in urinary isatin excretion during stress were investigated. This is the first study to demonstrate by HPLC that urinary isatin excretion is increased by stress. Both types of stress induced a marked increase in urinary isatin excretion during the 24 hr following the initiation of stress. Dexamethasone administration prevented the increase in urinary isatin excretion induced by both of the different types of stress. Furthermore, administration of either the benzodiazepine receptor agonist diazepam or the tyrosine hydroxylase inhibitor alpha-methyl-p-tyrosine prevented the increase in urinary isatin excretion induced by acute food deprivation, whereas the dopamine-beta-hydroxylase inhibitor diethyldithiocarbamate proved ineffective. These observations suggest that during stress, activated catecholamine-synthesizing cells and corticotropin-releasing factor cells, both of which play central roles in stress responses, may be involved in total isatin production. Isatin may serve as an endogenously generated marker for some types of stress.[1]References
- Stress-induced increase in urinary isatin excretion in rats: reversal by both dexamethasone and alpha-methyl-P-tyrosine. Tozawa, Y., Ueki, A., Manabe, S., Matsushima, K. Biochem. Pharmacol. (1998) [Pubmed]
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