Drugs online research references
Fundam Appl Toxicol. 1996 Mar;30(1):102-8.
The direct effect of hepatic peroxisome proliferators on rat Leydig cell function in vitro.
Liu RC, Hahn C, Hurtt ME.
Haskell Laboratory for Toxicology and Industrial Medicine, E. I. du Pont de Nemours and Company, Newark, Delaware 19714-0050, USA.
A review of the literature indicates that some compounds which produce hepatic peroxisome proliferation in rats also appear to produce Leydig cell adenomas, and some also affect the serum concentrations of testosterone and estradiol. Previous studies with the peroxisome proliferator ammonium perfluorooctanoate showed a direct effect on Leydig cells to alter steroidogenesis. It was therefore proposed that peroxisome proliferators in general may directly affect Leydig cell function to produce Leydig cell tumors by some undetermined mechanism. The present study investigated whether the following peroxisome proliferators directly affect Leydig cell function in vitro: 2,4-dichlorophenoxyacetic acid, ammonium perfluorooctanoate, acetylsalicylic acid, clofibric acid, ciprofibrate, gemfibrozil, tiadenol, tibric acid, trichloroacetic acid, trichloroethylene, and Wyeth 14,643. Leydig cells, isolated from adult Crl:CDBR rats (12-16 weeks old), were treated with peroxisome proliferator for 21 hr and the medium was assayed for estradiol. The function of the treated Leydig cell was evaluated by measuring the release of testosterone in response to human chorionic gonadotropin (hCG). In general, the peroxisome proliferators reduced the hCG-stimulated release of testosterone and either reduced or had no effect on the baseline release of testosterone. Of the 11 peroxisome proliferators, 8 increased the release of estradiol from Leydig cells treated for 1 day. Two more compounds were found to increase estradiol production when the treatment period was extended to 2 days. These effects were seen at noncytotoxic doses and at concentrations similar to those achieved in rat serum in dietary studies. The results suggest that peroxisome proliferators, as a class of compounds, directly modify the steroidogenic function of Leydig cells in vitro. Some of these compounds are known to produce Leydig cell tumors in rats, but this association has yet to be established for other peroxisome proliferators. This suggests that compounds which directly affect Leydig cell function in vitro may also induce Leydig cell tumors in vivo. Further investigations are necessary to address the mechanism for the in vitro effects on Leydig cells and to clarify the apparent relationship between peroxisome proliferator-induced changes in Leydig cell function and the development of Leydig cell tumors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8812244&dopt=Abstract
J Dermatol Sci. 1996 Nov;13(2):172-7.
Evaluation of the phototoxic properties of some hypolipidemics in vitro: fenofibrate exhibits a prominent phototoxic potential in the UVA and UVB region.
Diemer S, Eberlein-Konig B, Przybilla B.
Dermatologische Klinik und Poliklinik, Ludwig-Maximilians-Universitat, Munchen, Germany.
As some fibric acid derivatives have been reported to exhibit photosensitizing effects in vivo, the antilipemic drugs fenofibrate, bezafibrate, clofibrate, and gemfibrozil were tested for their phototoxic potential in vitro by a photohemolysis test using human erythrocytes and different irradiation sources. In this system only fenofibrate revealed strong phototoxic properties, which were dependent both on the drug concentration and the irradiation doses. Above a surface dose of 40 J/cm2 UVA of an UVA (320-400 nm)-rich irradiation source or 1.6 J/cm2 UVB/0.8 J/cm2 UVA of an UVB (280-320 nm)-rich irradiation source human red blood cells were completely photohemolysed in the presence of fenofibrate. Bezafibrate- and gemfibrozil-induced photohemolysis remained beneath 10%, and clofibrate showed no phototoxicity at all. As the phototoxic potential of fenofibrate lies in the UVB and UVA range, this might be of relevance with regard to clinical photosensitivity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8953418&dopt=Abstract
Fortschr Med. 1996 May 10;114(13):157-60.
[Gemfibrozil in the elderly. Effects on lipid metabolism]
[Article in German]
Brosche T, Kipfmuller G.
Lehrstuhl Innere Medizin-Gerontologie, Institut fur Gerontologie, Universitat Erlangen-Nurnberg.
METHODS: Twenty patients with mixed hyperlipidemia type IIb were treated for two weeks with the lipid lowering agent gemfibrozil at a dose of 900 mg/day. The mean age of the 10 younger ambulatory patients was 32.3 +/- 4.1 years, that of the 10 geriatric inpatients 76.9 +/- 7.1 years. Fasting blood samples were drawn from the patients on days 1, 7 and 14, and plasma lipids and apolipoproteins determined. In addition, the plasma phospholipids were isolated and the fatty acid composition determined by gas chromatography. RESULTS: After only two weeks treatment with gemfibrozil, triglyceride and phospholipid plasma levels were significantly decreased. The therapeutic effects were more pronounced in the elderly patients, mainly female and most with diabetes mellitus, than in the younger, predominantly male hyperlipidemic patients. In accordance with the mechanism of action of gemfibrozil, the initially pathologically elevated levels of plasma free fatty acids in the geriatrics returned to normal. Furthermore, the fraction of long chain saturated fatty acids among the phospholipids became smaller, suggesting an impairment of chain elongation of fatty acids in the hepatic microsomes.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8964557&dopt=Abstract
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