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

Effects of repeated administration of benthiocarb on the nitrogen metabolism of hepatic and neuronal systems have been studied. Repeated benthiocarb treatment was associated with significant decrease in proteins with a concomitant increase in free amino acids (FAA) and specific activity levels of proteases suggesting impaired protein synthesis or elevated proteolysis. The glycogenic aminotransferases showed a significant elevation in both the tissues indicating high feeding of ketoacids into oxidative pathway for efficient operation of TCA cycle to combat energy crisis during induced benthiocarb stress. However, the activity levels of branched-chain aminotransferases decreased suggesting their reduced contribution of intermediates to TCA cycle. A comparative evaluation of the activity levels of ammonogenic enzymes, AMP deaminase, adenosine deaminase and glutamate dehydrogenase (GDH) indicated that ammonia was mostly contributed by nucleotide deamination rather than by oxidative deamination. GDH exhibited reduced activity due to low availability of glutamate. In accordance with increased levels of urea, the activity levels of arginase, a terminal enzyme of urea cycle was increased suggesting increased urea cycle operation in order to combat the increased ammonia content. As the presence of urea cycle in the brain is rather doubtful, the conversion of ammonia to glutamine for the synthesis of GABA is envisaged in brain whereas in liver, excess ammonia was converted to urea through ornithine-arginine reacting system. The increased glutaminase activity observed during benthiocarb intoxication is accounted for counteracting acidosis or maintenance of metabolic homeostasis. Arginase, a terminal enzyme of ornithine cycle showed increased activity denoting the efficient potentiality of tissues to avert ammonia toxicity. The changes observed in tissues of rat administered with benthiocarb reflects a shift in nitrogen metabolism for efficient mobilization of end products of protein catabolism.
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PMID:Perturbations in nitrogen metabolism of brain and liver of rat following repeated benthiocarb administration. 266 46

By growing Aedes albopictus mosquito cells in media containing increasing concentrations of adenosine and subsequently plating low numbers of cells in the presence of EHNA (an inhibitor of adenosine deaminase), three clones were obtained which were resistant to adenosine. The adenosine-resistant clones contained level of adenosine and thymidine kinase similar to those in the parental cells, but were unable to incorporate labeled nucleotides (adenosine, uridine, thymidine, or guanosine) into TCA-precipitable material. The inability to incorporate nucleosides was also reflected in an enhanced resistance to several nucleoside analogs such as 5-fluorodeoxyuridine and tubercidin but not to the unribosylated base, 5-fluorouracil. Direct measurements over short time intervals indicated that the primary defect in these cells was at the level of nucleoside transport.
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PMID:Aedes albopictus cells resistant to adenosine because of a defect in nucleoside transport. 713 63