Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tissue accumulation of arginine (Arg), N-acetylarginine (NA), argininic acid (AA) and homoarginine (HA) occurs in hyperargininemia, an inborn error of the urea cycle. In the present study, we investigated the in vitro effects of Arg, NA, AA and HA on NTPDase1 and 5'-nucleotidase activities from synaptosomal cerebral cortex of rats. The results showed that Arg enhances NTPDase1 activity at the high concentrations tested (1.5 and 3.0mM) for both the ATP and ADP nucleotides. Activation was also observed with other guanidino compounds tested: NA, AA and HA activated ATP and ADP hydrolysis in all experiments at the concentration of 25 microM. Besides this, NA and AA activated ATP hydrolysis at a lower concentration (1 microM). In another set of experiments, we verified the effect of Arg on purified apyrase at pH 8.0 and 6.5 and observed an increase in the enzyme activity at all Arg concentrations tested (0.01-3.0mM). In contrast, Arg and the other guanidino compounds tested did not alter 5'-nucleotidase activity. These results suggest that changes in nucleotide hydrolysis may be involved in the brain dysfunction caused by hyperargininemia amongst other potential pathophysiological mechanisms involved in this condition.
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PMID:In vitro effects of L-arginine and guanidino compounds on NTPDase1 and 5'-nucleotidase activities from rat brain synaptosomes. 1261 83

Studies demonstrated that the iron chelating antioxidant restores brain dysfunction induced by iron toxicity in animals. Earlier, we found that iron overload-induced cerebral cortex apoptosis correlated with oxidative stress could be protected by naringenin (NGEN). In this respect, the present study is focused on the mechanisms associated with the protective efficacy of NGEN, natural flavonoid compound abundant in the peels of citrus fruit, on iron induced impairment of the anxiogenic-like behaviour, purinergic and cholinergic dysfunctions with oxidative stress related disorders on mitochondrial function in the rat hippocampus. Results showed that administration of NGEN (50 mg/kg/day) by gavage significantly ameliorated anxiogenic-like behaviour impairment induced by the exposure to 50 mg of Fe-dextran/kg/day intraperitoneally for 28 days in rats, decreased iron-induced reactive oxygen species formation and restored the iron-induced decrease of the acetylcholinesterase expression level, mitochondrial membrane potential and mitochondrial complexes activities in the hippocampus of rats. Moreover, NGEN was able to restore the alteration on the activity and expression of ectonucleotidases such as adenosine triphosphate diphosphohydrolase and 5'-nucleotidase, enzymes which hydrolyze and therefore control extracellular ATP and adenosine concentrations in the synaptic cleft. These results may contribute to a better understanding of the neuroprotective role of NGEN, emphasizing the influence of including this flavonoid in the diet for human health, possibly preventing brain injury associated with iron overload.
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PMID:Naringenin Mitigates Iron-Induced Anxiety-Like Behavioral Impairment, Mitochondrial Dysfunctions, Ectonucleotidases and Acetylcholinesterase Alteration Activities in Rat Hippocampus. 2605 Feb 8