Ionamin online research references
Exp Mol Pathol. 1983 Jun;38(3):368-79.
Chlorphentermine-induced alterations in the lungs of vitamin E-deficient and supplemented rats: 1. Biochemical and morphometric analysis of the pulmonary response.
Gairola C, Matulionis DH, Reasor MJ.
Male Sprague-Dawley rats were maintained on diets containing 0.60, or 300 ppm vitamin E (VE) for 9 weeks with chlorphentermine (CP) or saline vehicle (SV) treatments administered over the last 3 weeks (20 mg CP/kg for one week and 30 mg CP/kg for subsequent 2 weeks or equivalent volume of saline vehicle). Spontaneous erythrocyte hemolysis averaged 68% for VE-deficient (0 ppm) and less than 9% for VE-supplemented (60 and 300 ppm) animals prior to saline and CP treatments. These values were not changed significantly by vehicle or drug administration. The lung-to-body weight ratios nearly doubled and the total lung phospholipid levels increased equivalently (three- to fourfold) in all three CP-treated VE groups as compared to corresponding SV controls. The levels of thiobarbituric acid-reactive material (TBA-RM), an index of lipid peroxidation, was increased in the lung tissue above SV controls in all dietary groups with the deficient group being the highest. There was no difference in the TBA-RM values of 60 and 300 ppm groups within each group. Quantitative morphometric analysis revealed that in the VE-supplemented groups, CP treatment caused a significant increase in the number of alveolar macrophage foam cells (FC) with a slight increase in the volume density of surfactant-like material (SLM). By comparison, there were fewer FCs but a larger quantity of SLM in the VE-deficient group. The results suggest that VE deficiency modifies the pulmonary response to CP resulting in lipid peroxidation-induced FC disintegration and the accumulation of SLM.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6852209&dopt=Abstract
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Pharmacology. 1983;26(5):274-84.
Effect of chlorphentermine on the pulmonary clearance of 5-hydroxytryptamine in rabbits in vivo.
Mehendale HM, Morita T, Angevine LS.
Previous studies from this laboratory demonstrated that the pulmonary clearance of 5-hydroxytryptamine (5-HT) is perturbed by pulmonary accumulation of chlorphentermine (CP) by isolated perfused lung preparations. This observation raises the possibility that depressed 5-HT clearance may be one factor contributing to CP-induced pulmonary hypertension. The primary objective of the present studies was to determine if the effect of CP could be demonstrated in vivo during single-pass circulation through the lungs. Pulmonary extraction and metabolism of [14C]-5-HT during single pulmonary passage were examined using the reference indicator radioisotope dilution technique in male New Zealand albino rabbits. In control or saline vehicle injected animals, it was established that 81% of administered [14C]-5-HT was extracted by the lung and 25% of total radioactivity in the blood stream was recovered as 5-hydroxyindoleacetic acid (5-HIAA) during single passage through the lungs. Appropriate control incubations of 5-HT with blood and simulated pulmonary circulation through the extracorporeal circulation system yielded only 2 and 5% metabolism, respectively. These results indicate that significant pulmonary metabolism of 5-HT followed by efflux of 5-HIAA into venous output occurs during single-pass circulation. Preadministration of CP (0.5, 1 and 3 mg/kg single dose, i.v.) caused a dose-related inhibition of pulmonary extraction of 5-HT. This effect was also accompanied by a dose-related suppression of the appearance of the metabolite of 5-HT. These results provide in vivo evidence for impairment of pulmonary extraction and deactivation of 5-HT as a result of prior pulmonary accumulation of CP.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6856669&dopt=Abstract
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Fundam Appl Toxicol. 1983 May-Jun;3(3):192-8.
Impairment in pulmonary bioenergetics following chlorphentermine administration to rats.
Zychlinski L, Montgomery MR, Shamblin PB, Reasor MJ.
Biochemical alteration in pulmonary oxidative metabolism and morphological integrity of lung mitochondria were examined in rats following administration of chlorphentermine (30 mg/kg, ip, 5 days per week) for 1 or 2 weeks. During the first week of treatment, body weight gain and food intake were decreased markedly but returned to control levels during the second week. Phospholipid content of the lung was increased 31% and 110% after 1 and 2 weeks of treatment, respectively. This was accompanied by a striking intraalveolar accumulation of hypertrophic alveolar macrophages. The metabolism of both (1-14C)- and (6-14C)-glucose was decreased 27% and 26%, respectively, after 2 weeks of drug treatment. In rat lung mitochondria, chlorphentermine significantly lowered the RCR and ADP/O ratio and stimulated state 4 respiration. State 3 respiration and uncoupled state respiration were unaffected. These data indicate that chlorphentermine functions as a true uncoupler of oxidative phosphorylation when administered in vivo. Furthermore, disruption of mitochondrial membranes was observed frequently in lung mitochondria from treated animals. These combined data indicate that the induction of pulmonary phospholipidosis by chlorphentermine is accompanied by marked alterations in subcellular bioenergetics and mitochondrial structure.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6884634&dopt=Abstract
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