Ionamin online research references
Lab Invest. 1982 Feb;46(2):224-30.
Multinucleation in alveolar macrophages from rats treated with chlorphentermine.
Reasor MJ, Massey CA, Koshut RA, Castranova V.
When rats were treated with chlorphentermine, a cationic amphiphilic drug, a phospholipid storage disorder developed in alveolar macrophages, the severity of which was directly proportional to the duration of treatment over a 4-week period. Concomitantly, a progressively greater percentage of the cells became multinucleated such that, after 4 weeks of drug treatment, 18 per cent of the cells contained more than one nucleus. Greater than 99 per cent of the macrophages from control rats had on nucleus per cell. Associated with the multinucleation was an increase in the DNA, RNA, and protein content of the macrophages and increases in the RNA to DNA and protein to RNA ratios relative to cells from untreated rats. Centrifugal elutriation was employed as a means to study the multinucleation as a function of increasing cell size. At each of the 4 weekly intervals studied, the percentage of cells with two or more nuclei increased as the cells became larger. An increase in multinucleation was also found in cells of any given size range as the time of treatment increased. Possible mechanisms responsible for the multinucleation phenomenon are discussed.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6174825&dopt=Abstract
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Fundam Appl Toxicol. 1982 Nov-Dec;2(6):306-12.
Effect of chlorphentermine pretreatment on 5-hydroxytryptamine disposition in the isolated perfused rat lung.
Angevine LS, Mehendale HM.
Chlorphentermine (CP) is known to be highly accumulated by the lung, to cause pulmonary phospholipidosis and has been suspect in causing pulmonary hypertension possibly by inhibiting the clearance of 5-hydroxytryptamine (5-HT). It was of interest to determine if subacute CP treatment might inhibit 5-HT clearance by the lung. Animals were treated with CP (50 mg/kg/day po in saline) for 7 days while controls received the vehicle only. Artificially ventilated isolated rat lungs were perfused with a constituted medium. In recirculation perfusion experiments, lungs from CP treated animals exhibited both decreased uptake and metabolism of 14C-5-HT (0.02 microM). In order to distinguish between CP-induced morphological effects and the effect of CP itself, CP was added at an initial perfusate concentration of 0.5 or 5 mumol to the perfusate of lung from untreated animals. A dose-dependent inhibition of 5-HT uptake and metabolism was observed, such that lungs receiving 5 mumol of CP inhibited 5-HT metabolism similarly to that observed in treated lungs. In order to distinguish the effect of CP on 5-HT uptake from its effect on metabolism, pulmonary disposition of 5-HT was studied in the presence of pargyline, a monoamine oxidase (MAO) inhibitor known to block the metabolism of 5-HT. In the presence of 1 mM pargyline, CP (5 mumol) significantly decreased 5-HT uptake by the lung. CP was also noted to inhibit the metabolism of 14C-5-HT by in vitro incubations of 700 g lung supernatent fractions. In conclusion, subacute treatment with CP results in obtunded clearance of 5-HT by the rat lung, supporting the proposal that CP-induced pulmonary hypertension may be mediated by decreased pulmonary clearance of 5-HT.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6193024&dopt=Abstract
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Fed Proc. 1984 Aug;43(11):2586-91.
Pulmonary disposition and effects of drugs on pulmonary removal of endogenous substances.
Mehendale HM.
Pulmonary sequestration of drugs and other xenobiotics is known to affect respiratory and nonrespiratory functions of the lung and may be causally related to drug-induced pulmonary disease. We employed chlorphentermine (CP), an anorexic drug of amphiphilic physicochemical properties, to unravel possible mechanisms underlying drug-induced pulmonary hypertension associated with this class of drugs. In isolated perfused lungs, CP interferes with pulmonary clearance of 5-hydroxy tryptamine (5-HT) and norepinephrine. Pulmonary uptake and metabolism of 5-HT are inhibited by CP in rabbit and rat lungs. In in vitro incubations, CP is a powerful inhibitor of pulmonary monoamine oxidase activity. When pulmonary metabolism of 5-HT was blocked by pargyline, CP also inhibited pulmonary uptake of 5-HT. These effects of CP can be demonstrated in vivo in rabbits and rats during a single pulmonary passage of radio-labeled 5-HT. Not all pneumophilic drugs interfere with pulmonary clearance of 5-HT, as illustrated by the lack of effects by chlorpromazine and propranolol despite their pulmonary accumulation to a significant extent. Pulmonary accumulation of the chlorinated analogs such as chlomipramine and CP is greater than their nonchlorinated congenors, and this is in agreement with their ability to impede pulmonary clearance of 5-HT. These studies suggest that the electrophilic chlorine substitution increases the affinity of these chemicals for lung tissue, which increases the likelihood of their interference with the pulmonary disposition of 5-HT.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6204891&dopt=Abstract
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