Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Isocarboxazid”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

[Effects of beta-phenylethylamine derivatives on the central nervous system. (5) The effect of intracerebral administration of tyramine on head twitching in mice pre-treated with isocarboxazid].

Effects of drugs on head-twitches induced by tyramine (Ty) in isocarboxazide (Iso) pretreated mice were studied and the following results obtained: 1) In beta-phenylethylamine derivatives, p-hydroxyamphetamine in non-treated and Iso-pretreated mice and Ty in Iso-pretreated mice produced head-twitches. 2) Injection of 5-HTP (i.c. and i.p.) into mice induced head-twitches. 3) Although head-twitches were not induced by a low dose of 5-HTP (20 mg/kg, i.p.), in Iso pretreated mice, the number of headtwitches increased markedly in the Iso-Ty treated group when Ty was injected i.c. in Iso+5-HTP (20 mg/kg) pretreated mice. 4) When Iso-Ty was injected into alpha-methyl-p-tyrosine pretreated mice, the number of head-twitches increased markedly compared with Iso-Ty treated group. 5) When Iso-Ty was injected into mice sustained with p-chlorophenylalanine, the number of head-twitches decreased markedly compared with the Iso-Ty treated group. 6) The number of head-twitches decreased markedly when Iso-Ty was injected into dimetotiazine pretreated mice, however the administration of Iso-Ty in haloperidol pretreated mice had no influence on head-twitches. 7) It is concluded that serotonin is the acting mediator in the head-twitch response.

5-Hydroxytryptophan↗

Spectrophotometric determination of isocarboxazid bulk drug and tablets by reaction with p-dimethylaminocinnamaldehyde.

A spectrophotometric method is described for the determination of isocarboxazid. The method is based on the reaction of the drug with p-dimethylaminocinnamaldehyde in the presence of trichloroacetic acid in a methanolic medium to produce a very intense red chromophore (lambda max = 500 nm, Emax = 1.05 x 10(5]. The reaction is proposed to proceed via electrophilic attack at the C-4 position of the isoxazole nucleus. Job's plot indicated a 1:1 drug-to-reagent ratio. Regression analysis of Beer's plot showed excellent correlation (r = 0.9996) in the concentration range 0.25-2.10 micrograms isocarboxazid/mL. The developed color is stable for at least 12 h. Results of analyses of bulk drug and tablets by the proposed method are comparable to those for USP XXI methods.

Catalysis↗

The response of depressed inpatients to isocarboxazid.

Fifty-six inpatients with unipolar depression completed treatment with isocarboxazid. In comparing the differences between responders and nonresponders, it was found that psychomotor retardation, pathological guilt, daily persistence of unremitting symptoms, phobic anxiety, dexamethasone suppression test nonsuppression, and neuroticism were significantly more common among nonresponders. Reactivity of mood, blaming others, and extraversion were more common in responders. Total endogenous depression scores on the Newcastle 1, Newcastle 2, and Michigan scales were also significantly higher in nonresponders. Attained platelet monoamine oxidase inhibition was similar in both groups.

Adult↗

Mania after withdrawal of isocarboxazid.

Two cases of mania following the discontinuation of treatment with isocarboxazid are described. Although this phenomenon has been reported by several investigators to occur after cessation of tricyclic antidepressant therapy, there exists only one isolated report of hypomania after discontinuation of monoamine oxidase inhibitors. Possible mechanisms for the occurrence of hypomania and mania after withdrawal from antidepressants are discussed.

Adult↗

Inhibitory effect of leptophos on carboxylesterase (isocarboxazid amidase) in rat liver.

The organophosphate insecticide, leptophos, inhibited rat liver isocarboxazid amidase (ISOCase) activity to 20% of control at 5.0 mg/kg l h after administration, but at this dose brain cholinesterase (ChE) activity was not affected. The activity of ISOCase decreased to 29 and 0% of control 24 h after treatment with leptophos at doses of 2.5 and 5.0 mg/kg, respectively. With repeated administration of leptophos at a dose of 1 mg/kg for 10 days, ISOCase activity decreased to 34% of control on day 1 and the inhibition increased to 85% on day 10 without inhibition of brain ChE activity. After cessation of three successive daily doses (1 mg/kg/day), the ISOCase activity was gradually restored near to control levels in 8 days. Pretreatment with carboxylesterase inhibitors, triorthocresylphosphate (TOCP) and bis-p-nitrophenylphosphate (BNPP), potentiated the inhibition of brain ChE by leptophos, suggesting that ISOCase might take a role in leptophos detoxification.

Animals↗