Drugs online research references
Immunopharmacology. 1992 Jul-Aug;24(1):37-45.
Acetaminophen inhibits the human polymorphonuclear leukocyte function in vitro.
Shalabi EA.
Department of Physiology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
The aim of the study is to investigate the effect of Acetaminophen (Am) on the oxidative respiratory burst of isolated human polymorphonuclear leukocytes (PMNs). Acetaminophen inhibited the luminolchemiluminescence (CL) peak response of PMNs stimulated with phorbol myristate acetate (PMA) or opsonized zymosan in a concentration dependent manner. The inhibitory effect of Am on PMA-stimulated PMNs-CL response was partially reversible. The level of CL inhibition with Am plus the hydroxyl radical scavengers allopurinol, dimethyl sulfoxide (DMSO) or superoxide dismutase (SOD) is greater than that with Am alone. Generation of superoxide (O2-) by stimulated PMNs, as assayed by superoxide dismutase inhibitable reduction of Ferricytochrome c, was markedly inhibited by Am. Furthermore, the phagocytic activity of PMNs as tested for by the ingestion of opsonized dead yeast was significantly reduced in Am-treated cells. These results indicate clearly that Am causes significant inhibition of the human PMNs function in vitro.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1333457&dopt=Abstract
J Pharmacol Exp Ther. 1989 Jan;248(1):315-9.
Paraxanthine metabolism in humans: determination of metabolic partial clearances and effects of allopurinol and cimetidine.
Lelo A, Kjellen G, Birkett DJ, Miners JO.
Department of Clinical Pharmacology, Flinders Medical Center, Bedford Park, Adelaide, South Australia.
Paraxanthine (PX; 1,7-dimethylxanthine) is the major metabolite of caffeine in humans. Despite the continuous exposure of a large proportion of the population to PX, little is known about PX disposition in humans. The present study was performed to define the metabolic partial clearances of PX in humans and, by determining the effects of cimetidine and allopurinol pretreatments on PX disposition, assess the relative importance of cytochrome P-450 and xanthine oxidase in PX biotransformation. The combined formation of the 7-demethylated products 1-methylxanthine (1-MX), 1-methyluric acid (1-MU) and 5-acetyl-amino-6-formylamino-3-methyluracil (AFMU) accounted for 67% of PX clearance. Formation of 7-methylxanthine (7-MX) and 1,7-dimethyluric acid and renal excretion of unchanged PX comprised 6, 8 and 9% of PX clearance, respectively. Allopurinol pretreatment had no effect on PX plasma clearance but decreased 1-MU excretion and increased 1-MX excretion, with the combined excretion of these metabolites remaining constant. Cimetidine pretreatment decreased PX plasma clearance by 30%. Metabolic partial clearances to 1-MX + 1-MU and to AFMU were reduced to a similar extent (ca. 40%) in the cimetidine treatment phase, but other pathways were not significantly affected. These data are consistent with 1-MX and AFMU being derived from a common intermediate, the formation of which is mediated by cytochrome P-450. Xanthine oxidase catalyzes only the secondary conversion of 1-MX to 1-MU.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2913277&dopt=Abstract
J Clin Invest. 1988 Apr;81(4):1297-301.
Xanthine oxidase produces hydrogen peroxide which contributes to reperfusion injury of ischemic, isolated, perfused rat hearts.
Brown JM, Terada LS, Grosso MA, Whitmann GJ, Velasco SE, Patt A, Harken AH, Repine JE.
Department of Surgery, University of Colorado, Health Sciences Center, Denver 80262.
Three lines of investigation indicated that hydrogen peroxide (H2O2) from xanthine oxidase (XO) contributes to cardiac dysfunction during reperfusion after ischemia. First, addition of dimethylthiourea (DMTU), a highly permeant O2 metabolite scavenger (but not urea) simultaneously with reperfusion improved recovery of ventricular function as assessed by ventricular developed pressure (DP), contractility (+dP/dt), and relaxation rate (-dP/dt) in isolated Krebs-Henseleit-perfused rat hearts subjected to global normothermic ischemia. Second, hearts from rats fed tungsten or treated with allopurinol had negligible XO activities (less than 0.5 mU/g wet myocardium compared with greater than 6.0 mU/g in control hearts) and increased ventricular function after ischemia and reperfusion. Third, myocardial H2O2-dependent inactivation of catalase occurred after reperfusion following ischemia, but not after ischemia without reperfusion or perfusion without ischemia. In contrast, myocardial catalase did not decrease during reperfusion of ischemic hearts treated with DMTU, tungsten, or allopurinol.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3127425&dopt=Abstract
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