Drugs online research references
Ecotoxicol Environ Saf. 1994 Oct;29(1):13-9.
Evaluation of a rodent peroxisome proliferator in two species of freshwater fish: rainbow trout (Onchorynchus mykiss) and Japanese medaka (Oryzias latipes)
Scarano LJ, Calabrese EJ, Kostecki PT, Baldwin LA, Leonard DA.
Environ Corporation, Arlington, Virginia 22203.
Rainbow trout (Onchorynchus mykiss) and Japanese medaka (Oryzias latipes) were exposed to the hypolipidemic drug gemfibrozil, a known rodent peroxisome proliferator. Trout were injected (i.p.) daily for 2 weeks at doses of 0, 46, 87, or 152 mg/kg/day. Medaka were exposed to the nominal concentrations of 0, 1.25, 2.5, or 5 ppm in water for 2 weeks in a static-renewal system. Peroxisome proliferation was assessed by measuring fatty acyl-CoA oxidase (FAO) activity, peroxisomal bifunctional enzyme (PBE) quantity, and changes in liver-to-body weight ratios (LWR). Results indicate that a mild peroxisome proliferative response was observed in rainbow trout (significant increases in FAO activity at all dose levels and in LWR at the highest dose level). Medaka demonstrated a significant increase in PBE at the highest dose level, while nonsignificant increases in FAO activity were observed at the mid- and high-dose levels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7529160&dopt=Abstract
Cancer Lett. 1995 Nov 6;97(2):263-8.
Gemfibrozil-induced peroxisome proliferation and hepatomegaly in male F344 rats.
Sausen PJ, Teets VJ, Voss KS, Miller RT, Cattley RC.
Chemical Industry Institute of Toxicology, Research Triangle Park, NC 27709, USA.
Gemfibrozil is a widely used hypolipidemic drug in humans that causes peroxisome proliferation and hepatocarcinogenesis in rodents. The induction of hepatomegaly and hepatic peroxisome proliferation (measured as peroxisomal acyl CoA oxidase activity), was determined and compared to another peroxisome proliferator, WY-14,643 (0.1% in the diet) in male F344 rats. In a 21-day study, dietary no-observable-effect and lowest-observable-effect levels of gemfibrozil for both hepatomegaly and peroxisome proliferation were 0.002% and 0.005%, respectively. In a 42-day study, dietary concentrations of 0.9-2.0% gemfibrozil induced a similar magnitude of hepatomegaly to WY-14,643 (2.3-fold) but a higher level of peroxisome proliferation (16-18-fold) than the maximum induction for WY-14,643 (13-fold). The plateau in magnitude of gemfibrozil-induced peroxisome proliferation across the 0.9-2.0% dietary concentrations was associated with a plateau in serum concentration of gemfibrozil (approximately 20 micrograms/ml), similar to concentrations reported in human subjects receiving oral gemfibrozil. These results indicate that maximal induction of peroxisome proliferation by gemfibrozil can exceed that of a more potent compound such as WY-14,643, and further suggest that maximal induction of peroxisome proliferation can be limited by steady-state serum concentrations. Moreover, the reported lack of hepatic responses to gemfibrozil in humans is unlikely to be the result of inefficacy or unavailability of this drug, compared to other peroxisome proliferators, in rodents.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7497472&dopt=Abstract
Am Heart J. 1985 Nov;110(5):1107-15.
Nonpharmacologic and pharmacologic alteration of high-density lipoprotein cholesterol: therapeutic approaches to prevention of atherosclerosis.
Glueck CJ.
High-density lipoprotein (HDL) cholesterol, an independent coronary heart disease (CHD) risk factor, is inversely associated with CHD. Whether interventions to increase concentrations of HDL--particularly the HDL2, HDL3, and apolipoprotein A1 subfractions--will reduce the incidence of CHD in high-risk patients is thus an area of intense speculation. Both nonpharmacologic and pharmacologic regimens will raise HDL concentrations. Nonpharmacologic approaches include habitual high-level aerobic exercise and weight loss--both of these somewhat more effective in men than in women--cessation of cigarette smoking, and changing of dietary habits. A number of drugs have been found to elevate HDL cholesterol. These include the bile acid-binding resin cholestyramine, nicotinic acid, gemfibrozil, phenytoin, exogenous estrogens, and alcohol. Terbutaline has also been reported to raise HDL cholesterol. It is not yet known whether, and to what degree, pharmacologic and nonpharmacologic elevation of HDL cholesterol will retard or reverse the progression of atherosclerosis. Conversely, HDL cholesterol is lowered by a broad variety of drugs, including anabolic--androgenic steroids, exogenous progestins, and probucol, which are used therapeutically to reduce low-density lipoprotein (LDL) cholesterol. Some agents used to treat hypertension also reduce HDL cholesterol, especially thiazide diuretics and the beta blockers, with the possible exception of pindolol. In the antiadrenergic class of antihypertensive agents, reserpine and methyldopa lower HDL cholesterol, but the alpha blocker prazosin does not appear to affect HDL cholesterol. The alpha agonist guanabenz has no effect on HDL cholesterol, and the vasodilator carprazidil has been reported to raise HDL cholesterol. In light of these facts, investigations should be undertaken to determine whether the metabolic effects of antihypertensive agents blunt their beneficial effects on CHD.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2865887&dopt=Abstract
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