Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.7.1.2 (nitrate reductase)
 3,861 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic atrophic gastritis is considered a precancerous condition for carcinoma of the stomach. To evaluate the correlation between progressive alterations in the mucosa and gastric juice microenvironmental factors, retained involved on N-nitroso compounds carcinogenesis, detailed analyses of biochemical and microbiological parameters such as pH, total viable counts (TVC), nitrate reductase positive bacterial counts (NRPBC), nitrite (NO2-) and thiocyanate (SNC-) levels, were carried out on 56 fasting gastric juices samples obtained at endoscopy from 28 patients with chronic atrophic gastritis (CAG), 14 with gastric cancers (GC), and 14 normal controls (NC). The mean values of pH, nitrite, TVC, and NRPBC were significantly lower in the juices of NC than in those of CAG and GC patients. Furthermore, the mean levels of the same parameters were higher in GC than in CAG juices. No significant difference was found in the three groups for SCN- level which principally resulted influenced by smoke habit. The 28 patients with CAG were subdivided into two groups (Group A = Diffuse chronic atrophic gastritis--DCAG; Group B = Multifocal chronic atrophic gastritis--MCAG) according to the involvement of gastric corpus and fundus besides antrum by a process of mucosal atrophy. The mean levels of pH, nitrite, TVC, and NRPBC were significantly higher in MCAG than in normal controls but statistically lower in reference to DCAG and cancers. In these two groups no difference was found for the same variables. The percentage of contaminated juices was higher for DCAG and cancers in respect to MCAG but no difference was found between DCAG and neoplastic stomachs. The results of this study suggest that the DCAG could be considered as the chronic atrophic gastritis type more exposed to the risk of N-nitroso compounds carcinogenesis.
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PMID:Chronic atrophic gastritis and risk of N-nitroso compounds carcinogenesis. 328 75

The periplasmic nitrate reductase (NAP) from Paracoccus pantotrophus is a soluble two-subunit enzyme (NapAB) that binds two haem groups, a [4Fe-4S] cluster and a bis(molybdopterin guanine dinucleotide) (MGD) cofactor that catalyses the reduction of nitrate to nitrite. In the present study the effect of KSCN (potassium thiocyanate) as an inhibitor and Mo ligand has been investigated. Results are presented that show NAP is sensitive to SCN(-) (thiocyanate) inhibition, with SCN(-) acting as a competitive inhibitor of nitrate (K(i) approximately 4.0 mM). The formation of a novel EPR Mo(V) species with an elevated g(av) value (g(av) approximately 1.994) compared to the Mo(V) High-g (resting) species was observed upon redox cycling in the presence of SCN(-). Mo K-edge EXAFS analysis of the dithionite-reduced NAP was best fitted as a mono-oxo Mo(IV) species with three Mo-S ligands at 2.35 A (1 A=0.1 nm) and a Mo-O ligand at 2.14 A. The addition of SCN(-) to the reduced Mo(IV) NAP generated a sample that was best fitted as a mono-oxo (1.70 A) Mo(IV) species with four Mo-S ligands at 2.34 A. Taken together, the competitive nature of SCN(-) inhibition of periplasmic nitrate reductase activity, the elevated Mo(V) EPR g(av) value following redox cycling in the presence of SCN(-) and the increase in sulphur co-ordination of Mo(IV) upon SCN(-) binding, provide strong evidence for the direct binding of SCN(-) via a sulphur atom to Mo.
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PMID:Thiocyanate binding to the molybdenum centre of the periplasmic nitrate reductase from Paracoccus pantotrophus. 1110 96

Previously, it has been shown that treatment of Paracoccus denitrificans cells with phenylglyoxal inhibits the methyl-viologen-linked nitrate reductase activity by blocking the nitrate transporter. This inhibition disappears if tetraphenylphosphonium cation (TPP(+)) is added to the assay medium. In the present paper, the following evidence suggests that the effect of TPP(+) results from an increased transmembrane anion permeability and not from transporter reactivation or cell lysis. (1) Beside nitrate, TPP(+) also mediated the utilisation of chlorate, which normally lacks access to the cytoplasm. (2) The TPP(+) pathway had about hundred-times higher K(m) values for nitrate and chlorate than nitrate reductase in Triton X-100 permeabilised cells. (3) Although the uncoupler CCCP alone failed to overcome the PG block, it stimulated the operation of the TPP(+) pathway. (4) The method of continuous variations allowed the transport stoichiometry TPP(+)/NO(3)(-) to be determined as 3, indicating charge compensation for nitrate movement and the subsequent transmembrane two-electron redox reaction. Anion uptake was also measured independently from passive swelling of uncoupled spheroplasts in iso-osmotic solutions of ammonium salts. The permeability to nitrate lay in the permeability sequence Cl(-)<NO(3)(-)<ClO(4)(-)<SCN(-) and was further enhanced by TPP(+).
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PMID:Passive penetration of nitrate through the plasma membrane of Paracoccus denitrificans and its potentiation by the lipophilic tetraphenylphosphonium cation. 1261 55