Influence of steroids and stress on toxicity and disposition of tetraethylammonium bromide.
In female rats, pretreatment with dexamethasone acetate or triamcinolone reduced the toxicity and plasma concentrations of tetraethylammonium bromide while increasing its level in urine. Pretreatment with corticosterone acetate or pregnenolone-16alpha-carbonitrile shared none of these effects. Although starvation or restraint neither diminished the tetraethylammonium bromide concentrations in plasma nor accelerated its urinary excretion, its toxicity was diminished by the stress induced with spinal cord lesions, heat, cold, hydrocortisone, or reserpine as well as starvation or restraint. The protection offered against the toxicant by stress and by the potent glucocorticoids seemed to be mediated, at least partly, via different mechanisms. Stress-induced resistance to tetraethylammonium bromide could not be attributed to elevated plasma corticosterone levels, whereas glucocorticoid-induced resistance could be partially ascribed to increased urinary excretion of the toxicant.
D000818:Animals; D003345:Corticosterone / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D004347:Drug Interactions; D004409:Dyskinesia, Drug-Induced / Q000209:etiology; D005260:Female; D011285:Pregnenolone Carbonitrile / Q000494:pharmacology; D051381:Rats; D013256:Steroids / Q000494:pharmacology*; D013312:Stress, Physiological / Q000378:metabolism* / Q000503:physiopathology; D013757:Tetraethylammonium Compounds / Q000378:metabolism* / Q000633:toxicity; D014221:Triamcinolone / Q000494:pharmacology
D013256:Steroids; D013757:Tetraethylammonium Compounds; D011285:Pregnenolone Carbonitrile; D014221:Triamcinolone; D003907:Dexamethasone; D003345:Corticosterone