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

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