Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.4.4 (adenosine deaminase)
 5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immobilised inosine (6a) and adenosine (6c) and their 5'-phosphates have been synthesized. Reaction of the nucleosides with ethyl levulinate, followed by saponification or phosphorylation and then saponification, gave the 2',3'-O-[1-(2-carboxyethyl)ethylidene] derivatives 3 and 4 and the corresponding 5'-phosphates 2b and 2d. 6-Aminohexylagarose (5) was severally coupled to 2b, 2d, 3, and 4 through the carboxyl groups to give the polymers 6a-d. Adenosine deaminase converts 3 into 4, and 6c into 6a. The polymers can be used as affinity resins for adenosine deaminase, which is bound more strongly to 6c than to 6a. The operational capacity of 6a for adenosine deaminase is constant at 15--25 degrees, but decreases by approximately 16% from 25 degrees to 35 degrees. The resin 6a has been used to separate adenosine deaminase from mixtures containing other enzymes, for example, guanase or alcohol dehydrogenase.
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PMID:Substrate- and product-affinity resins for adenosine deaminase obtained by immobilisation of adenosine and inosine via 2',3'-cyclic acetal derivatives. 64 8

Brief exposure of primary cultures of hepatocytes to ethanol had a biphasic effect on glucagon receptor-dependent cyclic AMP (cAMP) production: 25-50 mM ethanol decreased cAMP levels, whereas treatment with 100-200 mM ethanol increased cAMP. This biphasic effect was also observed after pretreatment with 10 microM 4-methylpyrazole, an inhibitor of alcohol dehydrogenase. Adenosine A1 and A2 receptors in primary cultures of rat hepatocytes are coupled to inhibition and stimulation of adenylyl cyclase, respectively. Since primary cultures of hepatocytes release adenosine into their extracellular media, we tested whether the acute effects of ethanol on cAMP were mediated by extracellular adenosine. Co-incubation with 2 U/mL adenosine deaminase prevented inhibition of cAMP production by 25-50 mM ethanol, but had no effect on stimulation by 100-200 mM ethanol. Pretreatment of hepatocytes with 110 nM 8-cyclopentyl-1,3-dimethylxanthine, an adenosine A1 receptor antagonist, also completely blocked the inhibitory effects of ethanol on cAMP production. Low concentrations of ethanol enhanced the inhibitory effects of R(-)N6-(2-phenylisopropyl)adenosine, an A1 receptor agonist, on cAMP production in cells pretreated with adenosine deaminase to remove endogenous adenosine. These data suggest that endogenously produced adenosine can be an important modulator of the effects of ethanol on receptor-stimulated cAMP production in primary cultures of rat hepatocytes.
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PMID:Role of adenosine A1 receptors in inhibition of receptor-stimulated cyclic AMP production by ethanol in hepatocytes. 780 99

Topical application of ethanol to the gastrointestinal mucosa induces vasodilation. Using an in vivo microscopy technique, we studied the effect of topical ethanol on the submucosal microvessels that control mucosal blood flow in the rat stomach and identified vasoactive substances and receptors that mediate the ethanol vasoaction. Topical ethanol (1-20%) dilated submucosal arterioles dose dependently, but did not change venular diameters. An inhibitor of alcohol dehydrogenase, 1 mM 4-methylpyrazole, did not alter the ethanol vasoaction. Ethanol-induced arteriolar dilation was eliminated by adenosine deaminase, but other vasodilator inhibitors such as atropine, pyrilamine, indomethacin, human calcitonin gene-related peptide-(8-37), and N omega-nitro-L-arginine methyl ester did not prevent it. Ethanol-induced arteriolar dilation was inhibited by an adenosine A2-receptor antagonist, but not by an A1-receptor antagonist, whereas an A2-agonist, but not an A1-agonist, dose dependently dilated arterioles. Exogenous adenosine (10(-5)-10(-3) M) dilated arterioles to a similar extent as ethanol. This response was inhibited by an A2-antagonist. We conclude that nonmetabolized ethanol increases gastric mucosal blood flow via A2-receptors in submucosal arterioles.
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PMID:Adenosine A2-receptor mediates ethanol-induced arteriolar dilation in rat stomach. 899 46