Drugs online research references
No To Shinkei. 1989 Jun;41(6):575-81.
[Xanthine oxidoreductase activity in rat brain tissue: the changes after decapitation]
[Article in Japanese]
Oka H.
Department of Neurosurgery, Teikyo University School of Medicine, Tokyo, Japan.
Since only little xanthine oxidase (XO) activity in mammalian brain was detected in earlier reports, the major end product of AMP degradation in the brain has been believed to be hypoxanthine. Our recent experimental study however, has indicated the presence of uric acid in the rat brain subjected to focal ischemia or cold injury. Allopurinol, a xanthine oxidoreductase inhibitor, has been found to markedly suppress the uric acid production in the same experimental settings. These results suggested that uric acid is generated from hypoxanthine by enzymatic reaction in injured brain tissue. The aim of this experiment is to prove the existence of xanthine oxidoreductase activity in brain tissue. Xanthine oxidoreductase activity in rat cerebral tissue was measured immediately or at 24-hour after decapitation. Under pentobarbital anesthesia, twenty Sprague-Dawley rats were killed by decapitation following washout of the blood by trans-cardiac perfusion with cold physiological saline. Immediately or after 24 hours of decapitation ischemia, the forebrain was removed and homogenized in 6 ml ice cold 0.05 M potassium phosphate buffer (pH 7.8) containing 1 mM phenylmethylsulfonyl fluoride, 0.3 mM EGTA, and 10 mM dithiothreitol. The homogenate was centrifuged at 100,000 g for 60 min and then the supernatant was dialyzed overnight against 0.05 M potassium phosphate buffer (pH 7.8). Aliquot of each dialyzed supernatant (sample) and standard xanthine solution with NAD was reacted at 37 degrees C for 15 min to measure the combined activity of xanthine dehydrogenase (XDH) and XO. For the measurement of XO, standard xanthine solution without NAD was used.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2803824&dopt=Abstract
FEBS Lett. 1991 Oct 21;291(2):173-6.
Cytotoxicity of, and DNA damage by, active oxygen species produced by xanthine oxidase.
Chiricolo M, Tazzari PL, Abbondanza A, Dinota A, Battelli MG.
Departimento di Patologia Sperimentale, Universita di Bologna, Italy.
Toxicity to Raji cells of the xanthine oxidase/hypoxanthine system is related to the formation of single-strand DNA breaks. DNA damage was proportional to the concentration of xanthine oxidase and to the time of exposure. It was prevented by the absence of hypoxanthine, or by the presence of allopurinol, or both superoxide dismutase and catalase. The release of 51Cr from damaged cells was detectable 12 h after the inhibition of cloning efficiency and the production of DNA breakage. These data suggest that DNA damage induced by the oxygen products precedes the severe lesion to the cellular membrane.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1936259&dopt=Abstract
Ann Ital Chir. 1996 Jan-Feb;67(1):73-5.
[Effects of allopurinol on damage caused by ischemia and reperfusion of skeletal muscles: an in vivo spectroscopic analysis (31P-MR) in rats]
[Article in Italian]
Gurke L, Sutter PM, Kuhrmeier A, Erhard P, Martinoli S, Heberer M.
Reparto di chirurgia, Ospedale Civico, Lugano.
The effect of allopurinol on energetic metabolism (reutilization of hypoxanthine) has been studied in vivo by mean of 31P-RM spectroscopy on skeletal muscle in the rat in conditions of ischemia and reperfusion. The treatment with allopurinol demonstrates of on benefit or phosphocreatine and ATP kinetics. These results outline that reutilization of hypoxanthine doesn't represent a protective mechanism of allopurinol on skeletal muscles. The role of hypoxanthine reutilization has to be investigated with further researches.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8712621&dopt=Abstract
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