Neonatal toxicity in rats following in utero exposure to chlorphentermine or phentermine. The opposing effects of N-hydroxyamphetamine and N-hydroxyphentermine on the H2O2 generated by hepatic cytochrome P-450. Alveolar macrophage mediated pulmonary clearance suppressed by drug-induced phospholipidosis. Ionamin online references

Ionamin online research references

Toxicology. 1982;24(1):85-94.
Neonatal toxicity in rats following in utero exposure to chlorphentermine or phentermine.

Thoma-Laurie D, Walker ER, Reasor MJ.

The administration of chlorphentermine (30 mg/kg) to pregnant rats during the last 5 days of gestation resulted in the development of a phospholipidosis in the lungs of the dams. The disorder developed in utero, as the phospholipidosis was evident in the lungs of the neonates when examined at 12 h postpartum. In contrast, a phospholipidosis was not observed in the lungs of the dams or neonates following phentermine treatment (30 mg/kg). Concurrently, neonates of the chlorphentermine-treated dams displayed a significant decrease in body weight in comparison to controls. Between 16 h and 24 h postpartum, 83% of the neonates of chlorphentermine-treated dams died. Cross-fostering and starvation experiments revealed that the lethality was not due to aberrant maternal behavior by the chlorphentermine-treated dams or malnutrition of the neonates. Histological examinations revealed endothelial and septal alterations in the lungs of neonates from chlorphentermine-treated dams. No signs of toxicity, as evidenced by the maintenance of body weight, or lethality were observed in the neonates of the phentermine-treated dams.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7135406&dopt=Abstract

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Mol Pharmacol. 1982 Sep;22(2):465-70.
The opposing effects of N-hydroxyamphetamine and N-hydroxyphentermine on the H2O2 generated by hepatic cytochrome P-450.

Cho AK, Maynard MS, Matsumoto RM, Lindeke B, Paulsen U, Miwa GT.

The effects of N-hydroxyphentermine (NOHP) and N-hydroxyamphetamine (NOHA) on hydrogen peroxide generated by rat liver microsomes and reconstituted preparations in the presence of NADPH were compared. In microsome incubations, NOHP caused an increase in H2O2 levels and NOHA caused a substantial decrease. When the substances were compared for cytochrome P-450-dependent H2O2 generation in reconstituted preparations, NOHA at mM blocked generation and NOHP had no effect. NOHP appears to be an uncoupler of the cytochrome P-450 system in microsomes whereas NOHA is a potent inhibitor, presumably because of its ability to form a metabolic intermediate complex. During the course of their effects on O2 reduction, NOHP and NOHA are themselves undergoing oxidation, NOHP to 2-methyl-2-nitro-1-phenylpropane and NOHA to phenylacetone oxime. The enzymatic natures of these oxidations differ. Thus, two closely related arylalkylhydroxylamines differ substantially in their interaction with cytochrome P-450 systems.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7144739&dopt=Abstract

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Exp Lung Res. 1982 Dec;4(1):1-10.
Alveolar macrophage mediated pulmonary clearance suppressed by drug-induced phospholipidosis.

Ferin J.

Drug-induced phospholipidosis in rats treated with chlorphentermine (CP) for 4-7 days suppressed totally alveolar pulmonary clearance in the first days after a TiO2 aerosol exposure. Reversing phospholipidosis by treatment interruption led to a recovery of particle clearance. Morphological observations indicated that "foam cells" contained less TiO2 particles than alveolar macrophages (AM) of control rats. Clearance of ZnO particles which seems not to be mediated by AM was not affected by CP treatment. A grand average retention curve based on data from control groups of past experiments suggests that alveolar clearance of TiO2 particles has a phase 1 (T 1/2 = 7 days) lasting about 2 weeks and a phase 2 (T 1/2 = 69 days). The results with drug-induced phospholipidosis suggest that phase 1 is practically totally AM-mediated. Drug-induced phospholipidosis is a promising method for the study of AM involvement in defensive functions.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7169059&dopt=Abstract

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