Drugs online research references
Biochem Pharmacol. 1988 Dec 15;37(24):4697-705.
Inhibition of orotidylate decarboxylase by 4(5H)-oxo-1-beta-D-ribofuranosylpyrazolo[3,4-d] pyrimidine-3-thiocarboxamide (APR-TC) in B lymphoblasts. Activation by adenosine kinase.
Dee Nord L, Willis RC, Smee DF, Riley TA, Revankar GR, Robins RK.
Department of Biochemistry, Nucleic Acid Research Institute, Costa Mesa, CA 92626.
The nucleoside allopurinol riboside-3-thiocarboxamide (APR-TC; 4-(5H)oxo-1-beta-D-ribofuranosylpyrazolo[3,4,d]pyrimidine-3-thioca rboxamide) demonstrates potent in vitro antiviral activity against various DNA and RNA viruses and cytostatic activity against a variety of cell lines in culture. The IC50 for APR-TC in the splenic derived B lymphoblast cell line, WI-L2, was 0.3 microM. Adenosine kinase-deficient WI-L2 cells were resistant to growth inhibition by APR-TC, indicating that adenosine kinase (EC 2.7.1.20) is responsible for phosphorylation of APR-TC to form the monophosphate derivative (APR-TC-5'P). A 4-hr incubation of cells with 50 microM APR-TC resulted in severe depletion of intracellular pyrimidine nucleotide pools and the accumulation of 3 microM APR-TC-5'P. The cytotoxicity of APR-TC was reversed by uridine, indicating that the active form of this compound inhibits the de novo pyrimidine biosynthetic pathway. Further, APR-TC-treated cells could not utilize the pyrimidine nucleotide precursor [6-14C]orotic acid, suggesting that the UMP synthase complex is the major cellular site of inhibition. In studies utilizing cell-free lysates of WI-L2, chemically prepared APR-TC-5'P provided potent inhibition of the orotidylate decarboxylase activity (ODCase, EC 4.1.1.23) of the UMP synthase complex. APR-TC-5'P was competitive with OMP, and a Ki value of 0.35 nM was determined.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2849455&dopt=Abstract
J Pediatr Surg. 1990 Aug;25(8):917-21.
Prolonged survival and decreased mucosal injury after low-dose enteral allopurinol prophylaxis in mesenteric ischemia.
Megison SM, Horton JW, Chao H, Walker PB.
Department of Surgery, University of Texas Southwestern Medical Center, Dallas 75235-9031.
Previous studies demonstrating protective effects of allopurinol in intestinal ischemia have evaluated intravenous allopurinol (presently unavailable for human use) or enteral allopurinol at supranormal doses and, therefore, have questionable clinical relevance. To address this problem, we evaluated the protective effects of clinically used doses of enteral allopurinol in rats with intestinal ischemia. Forty male Sprague-Dawley rats (weighing 300 to 400 g) received enteral allopurinol (10 mg/kg) or water daily for 1 week. Rats were then subjected to superior mesenteric artery occlusion with interruption of collateral flow for 20 minutes to produce ischemic injury to the intestine. Segmental small bowel resections were performed in 10 control rats and 10 allopurinol-treated rats before and after reperfusion to identify histopathologic evidence of reperfusion injury. Mucosal injury was quantitated using a grading scale of 0 to 5 (5 being most severe). The remaining 20 rats (10 in each group) were observed for mortality (death within 7 days) after reperfusion. Mucosal injury after reperfusion was graded at 4.4 +/- 0.20 in controls versus 2.3 +/- 0.23 in the treated group (P less than .001). In addition, there was a significant increase in mucosal damage in the control group when postreperfusion specimens were compared with specimens taken before reperfusion (2.8 +/- 0.19 before and 4.4 +/- 0.20 after reperfusion, P less than .001). Injury score for the allopurinol-treated group did not significantly increase after reperfusion. Survival was 50% in the water-fed control group compared with 100% survival in allopurinol-treated rats (P = .016). We conclude that enteral allopurinol in the presently available form and dose is effective in reducing mesenteric reperfusion injury.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2401948&dopt=Abstract
Scand J Thorac Cardiovasc Surg. 1989;23(2):135-8.
Oxygen free radicals decrease survival time of isolated rat hearts.
Semb AG, Vaage J, Laumann JW, Klingen G, Ilebekk A.
Institute for Experimental Medical Research, University of Oslo, Norway.
Effects of oxygen free radicals (OFR), enzymatically generated in the coronary circulation, were studied in isolated rat hearts retrogradely perfused with Krebs-Ringer solution. Control hearts (n = 6) functioned adequately for at least 5 hours. When rat hearts (n = 6) received xanthine oxidase (XOD) and hypoxanthine (HX) in order to generate OFR, survival time was reduced to 31 +/- 0.4 min (mean +/- SEM). Infusion of XOD (n = 8) or HX (n = 5) alone also reduced cardiac survival time, to 32 +/- 6 min and 139 +/- 23 min, respectively. When allopurinol (an inhibitor of XOD) was given together with XOD (n = 6), survival time (277 +/- 30 min) was similar to the control value. The production of OFR did not result in depressed coronary flow or heart rate, but reduced the aortic pulse pressure. OFR thus can depress cardiac function and may ultimately cause cardiac arrest.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2749208&dopt=Abstract
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