Ionamin online research references
Fed Proc. 1985 Apr;44(7):2323-7.
Newborn response to cationic amphiphilic drugs.
Kacew S, Reasor MJ.
Administration of various cationic amphiphilic drugs in utero results in induction of a phospholipid storage disorder in many tissues, particularly in lungs. In addition to the phospholipidosis in utero, drug exposure results in toxicity to the offspring; newborn rats die within 48 h of birth. Although drug-induced pulmonary pathological changes appear to be involved in the observed mortality, this relationship remains unclear. In contrast to mammals, administration of cationic amphiphilic drugs to the chick embryo seems not to induce phospholipid storage in the tissues examined. Treatment of newborn rats directly with these drugs also induces phospholipidosis in several tissues including lung and kidney; however, mortality does not occur. Concurrent administration of phenobarbital and chlorphentermine reduces or prevents amphiphilic drug-induced phospholipid storage in newborn rat lung and kidney. Modification of chlorphentermine actions by phenobarbital may be caused by alterations in amphiphilic drug excretion, metabolism, and catabolic phospholipase activity. Evidence thus indicates that regardless of age, animals appear susceptible to the effects of cationic amphiphilic drugs; however, species and tissues examined, as well as specific drug administration, play an important role in the observed qualitative and quantitative responses.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2579857&dopt=Abstract
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Muscle Nerve. 1978 Sep-Oct;1(5):421-2.
Early changes in chlorphentermine myopathy of rat studied by freeze fracturing.
Schmalbruch H.
Chlorphentermine interferes with the metabolism of phospholipids. When administered to the rat in daily doses for 5 days, it causes necrosis of muscle fibers that are rich in mitochondria. Before the onset of necrosis, the following characteristics of freeze-fractured muscle preparations were observed: multilayered lipid globules and single-layered lipid membranes without membrane particles; different stages of exocytosis of lipid through the plasma membrane of the muscle fibers; and areas of plasma membrane that were devoid of particles of intramembranous proteins. These latter areas may arise secondary to exocytosis, to fusion of lipid vesicles with the plasma membrane, or to a direct action of chlorphentermine on the membrane. It is not known whether these areas give rise to membrane defects and fiber necrosis.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=263983&dopt=Abstract
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Xenobiotica. 1989 Mar;19(3):287-99.
Urinary and biliary metabolites of mephentermine in male Wistar rats.
Mori M, Uy N, Sakai K, Inoue M, Miyahara T, Kozuka H.
Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University, Japan.
1. Excretion of urinary and biliary radioactivity, and metabolites of [3H]mephentermine (MP), after i.p. or subcutaneous administration of [3H]MP to male Wistar rats, were determined by preparative t.l.c.-liquid scintillation counting. 2. About 45% of the radioactivity administered i.p. was excreted in the 24 h urine. The major urinary metabolite was conjugated p-hydroxymephentermine (p-hydroxy-MP), which accounted for about 18% of the administered radioactivity in the 24 h urine. 3. About 4.2% of the radioactivity administered subcutaneously was excreted in bile during 24 h. The major biliary metabolite was conjugated p-hydroxy-MP, which accounted for about 39% of the radioactivity excreted in the bile in 24 h. 4. Urinary and biliary minor metabolites detected were phentermine (Ph), p-hydroxyphentermine (p-hydroxy-Ph), N-hydroxyphentermine (N-hydroxy-Ph), N-hydroxymephentermine (N-hydroxy-MP) and their conjugates, and conjugated MP. 5. The conjugates were considered to be glucuronides from the inhibitory effect of saccharic acid 1,4-lactone on their hydrolysis with beta-glucuronidase. 6. Biliary excretion rates of conjugated p-hydroxy-Ph and p-hydroxy-MP reached maxima at 3 to 4 h, and non-conjugated metabolites were maximal at 1 to 2 h, after administration. 50% of the biliary metabolites was excreted within 5 h.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2665325&dopt=Abstract
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