Ionamin online research references
J Pharmacol Exp Ther. 1986 Jan;236(1):60-4.
Role of the alveolar macrophage in the induction of pulmonary phospholipidosis by chlorphentermine. II. Drug uptake into cells in vitro.
Heyneman CA, Reasor MJ.
This study was conducted to further assess the role of the alveolar macrophage in the induction of pulmonary phospholipidosis by the cationic amphiphilic drug, chlorphentermine (CP). Alveolar macrophages were collected from normal rats by pulmonary lavage, allowed to attach to glass cover slips and incubated with CP in vitro at 37 degrees C. The uptake of CP was measured using [14C]CP. Uptake is rapid, reaching equilibrium by 2 min resulting in the concentration of CP within the cells. The process is temperature-dependent being depressed markedly at 2 degrees C. Two components of uptake were identified. Below 0.2 mM CP, a carrier-mediated mechanism and diffusion are involved whereas, at concentrations above 0.2 mM, the carrier is saturated and diffusion predominates, with the intracellular binding of CP to membranes probably responsible for the striking sequestration. The carrier-mediated component obeys Michaelis-Menten kinetics, does not appear to require Na+ and is not affected by metabolic inhibitors. This is consistent with the concept that the process occurs by facilitated diffusion. Metabolism of CP does not play a role in the accumulation of the drug. The transport system is different from those involved in glucose, nucleoside or amino acid uptake. Total initial uptake was inhibited by the three cationic amphilic drugs tested, iprindole, chlorcyclizine and imipramine indicating that cationic amphiphilic drugs may share a common uptake system.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3941401&dopt=Abstract
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Arzneimittelforschung. 1986;36(1):134-7.
The influence of diuretics on the excretion and metabolism of doping agents. II. Phentermine.
Delbeke FT, Debackere M.
The urinary excretion of phentermine in humans was followed over a period of several days after the oral administration of two formulations. The intake of phentermine in a capsule generally resulted in an excretion peak 4 h after the administration followed by a second peak 12 or 24 h post dosing. The total amount excreted during 72 h varied from 62.7 to 84.8%. Concerning the administration of Ionamine 15, a sustained release formulation, the maximal excretion rate was spread over 3-9 h, while more than 85% of phentermine were excreted after 72 h. The excretion was affected by urinary pH. The intake of acetazolamide shortly after phentermine resulted in a decrease of the phentermine excretion during one day and in one subject in a suppression below the detection limit 4 h post dosing. The administration of furosemide or bumetanide produced only a diluting effect during 2 h.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3954816&dopt=Abstract
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J Pharmacol Exp Ther. 1985 Jan;232(1):239-43.
Gentamicin or chlorphentermine induction of phospholipidosis in the developing organism: role of tissue and species in manifestation of toxicity.
Kacew S.
Daily, s.c. injection of gentamicin (100 mg/kg) for 2 days produced a significant increase in total phospholipid content of newborn rat kidney. Separation of individual phospholipid components revealed a significant rise in renal phosphatidylserine, phosphatidylinositol and phosphatidylcholine, whereas no marked change was noted in sphingomyelin, phosphatidylethanolamine or phosphatidylglycerol. Gentamicin did not significantly alter individual phospholipid classes and total phospholipid content in newborn rat liver and lung. Daily, oral chlorphentermine (60 mg/kg) administration also elevated total renal phospholipid levels and all individual phospholipid classes except sphingomyelin. In addition, a significant rise in all phospholipid components and total phospholipid content was noted in lungs of chlorphentermine-treated newborns. In the case of rat kidney, both gentamicin and chlorphentermine produced the greatest percentage of increase in phosphatidylinositol, whereas in lung phosphatidylcholine exhibited the highest percentage of elevation in response to chlorphentermine. In newborn rat liver, chlorphentermine did not induce alterations in individual and total phospholipid content. Gentamicin or chlorphentermine (1 mg/egg) failed to induce a phospholipidosis in chick embryo kidney and liver. Evidence suggests that drug-induced phospholipidosis is both species- and tissue-dependent and that this metabolic phenomenon is associated with inhibition of lysosomal phospholipases.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3965695&dopt=Abstract
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