Ionamin online research references
Drug Metab Dispos. 1985 Mar-Apr;13(2):192-6.
Prevention of chlorphentermine-induced pulmonary phospholipidosis in rats by phenobarbital.
Reasor MJ, Davis ME.
It has been shown previously that the induction of pulmonary phospholipidosis in rats by chlorphentermine (CP) is essentially prevented by the concurrent administration of phenobarbital (PB). This study was conducted to investigate the mechanism(s) responsible for this protection. Male Long-Evans hooded rats received either 14C-CP (30 mg/kg, ip) or both PB (30 mg/kg, po) and the 14C-CP daily for up to 1 week. Associated with the PB-induced prevention of phospholipid accumulation in the lungs was an 84% reduction in CP content in the tissue. Excretion in urine and feces was 55 and 6%, respectively, of the administered 14C for the CP group, and 66 and 11%, respectively, for the CP + PB group. Increased urinary excretion was not due to enhanced glomerular filtration or urine output. With each group, nearly 80% of the 14C was extracted into ether from alkalinized urine and co-chromatographed on TLC with pure CP. The difference in nonextractable 14C (presumably polar metabolites of CP) between the two groups is small and cannot account for the difference in total 14C excreted in the urine. All of the fecal 14C was CP. These experiments rule out an increase in CP metabolism as the primary basis for the CP-induced enhancement in 14C excretion. PB appears to actually protect against CP-induced pulmonary phospholipidosis rather than reversing it. This occurs by an enhancement in excretion of CP, thereby preventing it from reaching levels in the lungs which lead to PL accumulation.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2859167&dopt=Abstract
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Comp Biochem Physiol C. 1985;82(2):389-94.
Chlorphentermine inhibits pulmonary mitochondrial monoamine oxidase.
Zychlinski L, Montgomery MR.
Oxidation of six amine substrates by rat, rabbit and guinea-pig lung mitochondrial monoamine oxidase (MAO) was investigated polarographically with a Clark oxygen electrode in the presence of chlorphentermine (CP). This amphiphilic drug decreased the deamination of serotonin, norepinephrine, tyramine and dopamine significantly in all three species. However, the oxidation of tryptamine and benzylamine was unchanged. Amine oxidation by MAO in guinea-pig lung mitochondria was much more sensitive to the CP-mediated inhibition than rat or rabbit. A kinetic study of serotonin oxidation in the absence and presence of CP showed that both Vmax and Km were affected. These combined data indicate that CP is a specific inhibitor of pulmonary, mitochondrial monoamine oxidase form A with mixed-type inhibition.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2866910&dopt=Abstract
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J Pharmacol Exp Ther. 1987 Jun;241(3):817-25.
Amphetamine-like effects of anorectics and related compounds in pigeons.
Evans SM, Johanson CE.
Four pigeons were trained to discriminate injections of d-amphetamine (AMPH; 2.0 mg/kg i.m.) from saline with responding maintained under a fixed-ratio 30 schedule of food delivery. When drugs used therapeutically as anorectics were tested, they consistently produced greater than 80% of AMPH-appropriate responding. The order of potency for substituting for AMPH was: mazindol greater than AMPH = phenmetrazine = phentermine greater than chlorphentermine = phendimetrazine = diethylpropion greater than clortermine = mefenorex. Other anorectics such as phenylpropanolamine (0.3-30.0 mg/kg) and fenfluramine (1.0-17.0 mg/kg) only substituted partially for AMPH whereas benzphetamine (1.0-100.0 mg/kg) resulted primarily in saline-appropriate responding. Compounds related to AMPH in biochemical mechanism of action or psychomotor stimulant activity also were tested. Methylphenidate (0.1-3.0 mg/kg), piribedil (0.3-17.0 mg/kg) and nisoxetine (0.03-1.0 mg/kg) shared discriminative stimulus properties with AMPH whereas bupropion (1.0-30.0 mg/kg) and propylhexedrine (10.0-100.0 mg/kg) substituted for AMPH in two of three pigeons tested. In contrast, caffeine and fenetylline resulted principally in saline-appropriate responding. Compounds from pharmacological classes not related to AMPH, such as morphine, diazepam and phencyclidine, failed to substitute for AMPH. In general, compounds with anorectic and/or stimulant properties shared discriminative stimulus properties with AMPH.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2885408&dopt=Abstract
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