Drugs online research references
Biol Chem Hoppe Seyler. 1991 Jan;372(1):35-41.
Reoxygenation injury in rat hepatocytes: mediation by O2/H2O2 liberated by sources other than xanthine oxidase.
de Groot H, Brecht M.
Institut fur Physiologische Chemie I, Heinrich-Heine-Universitat Dusseldorf.
The mechanism of reoxygenation injury was studied in primary cultures of isolated hepatocytes from rat liver. Reoxygenation injury, which affected up to 80% of the hepatocytes, was only inducible within a certain time window of the anaerobic incubation. Reintroduction of oxygen before this vulnerable period ensured the survival of the hepatocytes. After the vulnerable period upon reintroduction of oxygen the hepatocytes continued to die in the same way as the anaerobic control. Allopurinol had no effect on reoxygenation injury. From the inhibitors of the mitochondrial respiratory chain, both cyanide and antimycin A increased injury while rotenone was without significant effect on injury. Reoxygenation injury was significantly diminished by superoxide dismutase, but not by catalase. When added together, superoxide dismutase and catalase completely prevented reoxygenation injury. The results demonstrate that reoxygenation injury in hepatocytes is mediated by the combined action of both O2- and H2O2. These reduced oxygen species are not liberated by xanthine oxidase but possibly originate from the mitochondrial respiratory chain.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2039603&dopt=Abstract
Eur Surg Res. 1989;21(6):297-304.
Oxygen free radical-induced histamine release during intestinal ischemia and reperfusion.
Boros M, Kaszaki J, Nagy S.
Institute of Experimental Surgery, Szent-Gyorgyi Albert Medical University, Szeged, Hungary.
Acute mesenteric ischemia is highly lethal and therefore a serious problem for surgery and intensive care medicine; accordingly its pathophysiology warrants further study. Oxygen free radicals (OFR) play a role in the intestinal mucosal damage that develops during reperfusion after ischemia. Histamine (H) is generally released in various types of tissue ischemia. The link between H release and OFR has only been studied in in vitro systems. We tested the hypothesis that OFR may be involved in H release following reperfusion of the ischemic gut. The artery supplying a segment of the ileum was occluded for 1 or 2 h in anesthetized dogs. On reperfusion, a release of H into the venous effluent of the segment was demonstrated. Pretreatment of the animals with allopurinol (an inhibitor of xanthine oxidase), or with MTDQ-DA [6,6'-methylene-bis(2,2-dimethyl-4-methanesulfonic acid sodium-1,2-dihydroquinoline)], a superoxide anion scavenger, or with a combination of allopurinol and MTDQ-DA resulted in an inhibition of H release. We conclude that OFR may play a role in the local H release following intestinal ischemia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2483833&dopt=Abstract
Clin Pharmacol Ther. 1989 May;45(5):487-94.
H2-antagonist inhibition of human neutrophil superoxide anion synthesis.
Zimmerman J, Millard J.
Division of Critical Care, University of Wisconsin Children's Hospital, Madison.
In the mmol/L concentration range, cimetidine and ranitidine suppress superoxide anion generation by isolated intact human neutrophils. However, at normal pharmacologic concentrations in the mumol/L range, even prolonged exposure of neutrophils to these agents has no demonstrable effect on toxic oxygen species synthesis. In vitro inhibition does not involve neutrophil activation-densensitization or neutrophil cytotoxicity and is reversible to a great extent by drug washout. In the examination of possible free-radical scavenging action of these drugs, it was demonstrated that both drugs inhibit superoxide anion production by xanthine oxidase but not by chelated iron. This raises the possibility that these agents may bear structural similarities to oxypyrazolopyrimidines such as allopurinol.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2541961&dopt=Abstract
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