Drugs online research references
Metabolism. 2000 Apr;49(4):479-85.
Gemfibrozil metabolite inhibits in vitro low-density lipoprotein (LDL) oxidation and diminishes cytotoxicity induced by oxidized LDL.
Kawamura M, Miyazaki S, Teramoto T, Ashidate K, Thoda H, Ando N, Kaneko K.
Department of Internal Medicine, Tokyo Teishin Hospital, Japan.
We hypothesized that M1, a metabolite of gemfibrozil, may have antioxidant properties because of its hydroxylated phenol ring, 5-(4-hydroxy-2,5-dimethyl-phenoxy)-2,2-dimethyl pentanoic acid. The susceptibility of low-density lipoprotein (LDL) to oxidative modification was investigated by a method using 2,2-azobis(4-methoxy-2,4-dimethylvaleronitrile [MeO-AMVN]) or Cu2+ as previously reported. Conjugated dienes (CDs), lipid hydroperoxide (LPO), and thiobarbituric acid-reactive substances (TBARS) were measured to evaluate the degree of LDL oxidation. Oxidized LDL (OxLDL), which is used for cytotoxicity studies, was prepared by the dialysis method using Cu2+ as the oxidation inducer. Cytotoxicity induced by OxLDL was studied in J774 macrophages by colorimetric assay using 3-[4,5-dimethyl-thiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT assay). The oxidative modification of LDL was inhibited by M1 in a dose-dependent manner. The antioxidant effect of M1 on LDL oxidation was diminished by dialysis of the LDL incubated with M1 against phosphate-buffered saline (PBS), suggesting that M1 is hydrophilic rather than lipophilic. M1 diminished the cytotoxicity induced by OxLDL, although it was milder versus probucol. These data suggest that this gemfibrozil metabolite has an antioxidant effect on LDL, and thus M1 may contribute to the antiatherogenic effects of gemfibrozil.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10778872&dopt=Abstract
Atherosclerosis. 1986 Jan;59(1):95-8.
Gemfibrozil increases both apo A-I and apo E concentrations. Comparison to other lipid regulators in cholesterol-fed rats.
Krause BR, Newton RS.
HDL cholesterol (HDL-C) was increased by gemfibrozil (+3.6-fold), fenofibrate (+1.3-fold) and ciprofibrate (+1.2-fold) but not clofibrate or bezafibrate when dosed PO at 50 mg/kg for 2 weeks in cholesterol-fed rats. Cholesterol in apo B-containing lipoproteins decreased with gemfibrozil (-76%), clofibrate (-12%) and ciprofibrate (-12%). Plasma apo B decreased to the greatest extent with gemfibrozil (-86%) followed by ciprofibrate (-47%), fenofibrate (-40%), clofibrate (-24%) and bezafibrate (-20%). Only gemfibrozil increased plasma apo E levels which are characteristically low in this rat model. Gemfibrozil, fenofibrate and ciprofibrate increased apo A-I concentrations. It is concluded that plasma lipid regulators which elevate HDL in this model might do so by altering the metabolism and hence plasma concentration of apoAI (fenofibrate, ciprofibrate) or both apo E and A-I (gemfibrozil). It is hypothesized that drugs which alter the metabolism of both HDL peptides result in the greatest HDL-C elevation in the rat.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3081014&dopt=Abstract
Int J Pharm. 2000 Apr 25;200(1):59-66.
Macromolecular prodrugs. VIII. Synthesis of polymer-gemfibrozil conjugates.
Lovrek M, Zorc B, Boneschans B, Butula I.
Faculty of Pharmacy and Biochemistry, University of Zagreb, Croatia.
Gemfibrozil is covalently linked to two similar polymers: poly[alpha,beta-(N-2-hydroxyethyl-DL-aspartamide)] and poly[alpha,beta-(N-3-hydroxypropyl-DL-aspartamide)]. The synthesised polymer drug conjugates differ in average molecular mass, type of covalent bonding, length of spacer, drug-loading and solubility.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10845686&dopt=Abstract
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