Drugs online research references
Br J Pharmacol. 1995 Apr;114(7):1351-8.
Selective modification of rat hepatic microsomal fatty acid chain elongation and desaturation by fibrates: relationship with peroxisome proliferation.
Alegret M, Cerqueda E, Ferrando R, Vazquez M, Sanchez RM, Adzet T, Merlos M, Laguna JC.
Dept. Farmacologia y Quimica Terapeutica, Facultad de Farmacia, Nucleo Universitario de Pedralbes, Barcelona, Spain.
1. The time-course of the effect of clofibrate (CFB), bezafibrate (BFB) and gemfibrozil (GFB) on lipid plasma levels and palmitoyl-, palmitoleoyl- and gamma-linolenoyl-CoA elongase, delta-9, delta-6 and delta-5 desaturase activities, and microsomal electron transport chains, as well as the correlation with the peroxisomal proliferation phenomenon have been studied in male Sprague-Dawley rats. 2. As reported in our previous work, the three drugs behave as peroxisomal proliferators (the order of potency was BFB > CFB > or = GFB) and induced a clear reduction in both plasma cholesterol and triglyceride levels. 3. Palmitoyl-CoA elongation activity was increased by the three drugs (BFB = GFB > CFB), whereas palmitoleoyl-CoA elongation activity was only enhanced by GFB. Elongation activity was not modified by fibrates when gamma-linolenoyl-CoA was used as substrate. These results are in accordance with the existence of three different elongation systems for saturated, mono- and polyunsaturated fatty acids. 4. delta-9, delta-6 and delta-5 desaturase activities were increased by the three fibrates, with an order of potency BFB > CFB = GFB for delta-9 and delta-5, and GFB > BFB = CFB for delta-6. 5. Of the enzyme activities integrated in the microsomal electron transport chains, NADH cytochrome b5 reductase was not affected by fibrate treatment, NADPH cytochrome c reductase activity was enhanced (BFB = GFB > CFB), whereas NADH cytochrome c reductase activity was reduced by CFB and BFB.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7606338&dopt=Abstract
Atherosclerosis. 1991 Dec;91(3):257-65.
Inhibition of HMG-CoA reductase in mononuclear cells during gemfibrozil treatment.
Stange EF, Osenbrugge M, Rustan M, Reimann F, Schneider A, Ditschuneit HH, Ditschuneit H.
Department of Internal Medicine II, University of Ulm, Germany.
The effect of gemfibrozil treatment (900 mg/day) on serum levels of total cholesterol, HDL-cholesterol, triglyceride, apoproteins A-I, A-II and B as well as HMG-CoA reductase in mononuclear cells was studied in patients with hyperlipoproteinemia types IIa and IIb. After 4 weeks of treatment gemfibrozil reduced total serum cholesterol (IIa: -17%, IIb: -26%), triglyceride (IIa: -39%, IIb: -47%) and apoprotein B (IIa: -22%, IIb: -15%). HDL cholesterol was increased by 20-22% and apoproteins A-I and A-II by 4-11%. Concomitantly, HMG-CoA reductase activity in freshly isolated mononuclear cells was suppressed by 78% in type IIa and 51% in type IIb patients. Continuation of treatment for up to 16 weeks prompted a further decline to 8 and 5% of the initial values, respectively. However, gemfibrozil failed to affect HMG-CoA reductase directly in homogenized or cultured mononuclear cells and did not further promote the suppressive action of LDL when added to the culture medium. Similarly, preincubation with the drug did not significantly modulate the binding or degradation of LDL in the cultured cells. However, LDL from patients with hyperlipoproteinemia types IIa and IIb exhibited enhanced binding and more potent HMG-CoA reductase suppression when isolated after compared to before gemfibrozil treatment. It is suggested that the HMG-CoA reductase inhibition observed in mononuclear cells during gemfibrozil treatment is due to changes in LDL structure affecting LDL receptor binding rather than direct effects of the drug on cellular cholesterol metabolism.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1789808&dopt=Abstract
Fundam Appl Toxicol. 1987 May;8(4):454-64.
Experimental studies on reproduction with the lipid-regulating agent gemfibrozil.
Fitzgerald JE, Petrere JA, de la Iglesia FA.
Gemfibrozil, a new lipid-regulating agent, was evaluated in rats and rabbits for effects on various phases of the reproduction process. In teratology studies groups of pregnant rats and rabbits received gemfibrozil at doses up to 200 mg/kg during organogenesis (rat, Days 6-15; rabbit, days 6-18). For peri- and postnatal studies, groups of pregnant rats were given 92 or 331 mg/kg from Day 15 of gestation through weaning. In fertility studies groups of sexually mature male rats were given 93 or 326 mg/kg of gemfibrozil for 61 days and females were given 94 or 318 mg/kg for 15 days prior to mating within treatment groups. Drug administration continued in females through gestation and weaning of the F1 offspring. In subsequent fertility experiments, treated male rats were mated with untreated females and treated females were cohabitated with untreated males. Gemfibrozil did not elicit a teratogenic response in either rats or rabbits up to doses that resulted in maternal toxicity. Reduced pup weights during the neonatal and weaning periods in the female fertility study as well as in the perinatal-postnatal study were the only apparent drug effect. Treatment of female rats prior to mating had no significant effects on general reproductive parameters. Male rats given doses of about 300 mg/kg/day showed inconsistent and equivocal lower rates of fertility relative to the concurrent controls. No adverse effects were seen in the reproductive performance of offspring of gemfibrozil-treated male rats.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3475229&dopt=Abstract
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