Rinaldo Serena, Brunori Maurizio, Cutruzzolà Francesca
Dipartimento di Scienze Biochimiche A. Rossi Fanelli, Sapienza-Università di Roma, P.le A. Moro, 5 00185 Rome, Italy.
Biochem Biophys Res Commun. 2007 Nov 23;363(3):662-6. doi: 10.1016/j.bbrc.2007.09.036. Epub 2007 Sep 20.
Nitrite reductase (cd1NIR) from Pseudomonas aeruginosa, which catalyses the reduction of nitrite to nitric oxide (NO), contains a c-heme as the electron acceptor and a d1-heme where catalysis occurs. Reduction involves binding of nitrite to the reduced d1-heme, followed by dehydration to yield NO; release of NO and re-reduction of the enzyme close the cycle. Since NO is a powerful inhibitor of ferrous hemeproteins, enzymatic turnover demands the release of NO. We recently discovered that NO dissociation from the ferrous d1-heme is fast, showing that cd1NIR behaves differently from other hemeproteins. Here we demonstrate for the first time that the physiological substrate nitrite displaces NO from the ferrous enzyme, which enters a new catalytic cycle; this reaction depends on the conserved His369 whose role in substrate stabilization is crucial for catalysis. Thus we suggest that also in vivo the activity of cd1NIR is controlled by nitrite.
来自铜绿假单胞菌的亚硝酸还原酶(cd1NIR)催化亚硝酸盐还原为一氧化氮(NO),它含有一个c-血红素作为电子受体和一个发生催化作用的d1-血红素。还原过程包括亚硝酸盐与还原态的d1-血红素结合,随后脱水生成NO;NO的释放和酶的再还原完成循环。由于NO是亚铁血红素蛋白的强力抑制剂,酶促周转需要释放NO。我们最近发现,NO从亚铁d1-血红素上的解离速度很快,这表明cd1NIR的行为与其他血红素蛋白不同。在此我们首次证明,生理底物亚硝酸盐会将NO从亚铁酶上置换下来,从而进入一个新的催化循环;该反应依赖于保守的His369,其在底物稳定中的作用对催化至关重要。因此我们认为,在体内cd1NIR的活性也受亚硝酸盐控制。