Sreider C M, Grinblat L, Stoppani A O
Centro de Investigaciones Bioenergéticas, Facultad de Medicina, Buenos Aires, Argentina.
Biochem Int. 1992 Oct;28(2):323-34.
In order to elucidate the mechanism of the biological activation of nitrofurans, the interaction of these compounds with lipoamide dehydrogenase (LipDH)** was investigated. LipDH catalysed one-electron reduction of several nitrofuran derivatives. The reaction could be demonstrated spectroscopically and was enhanced by cadmium, arsenite and anaerobiosis. The role of flavin in the nitroreductase activity was supported by (a) the nitrofuran effect on the spectral properties of anaerobic, arsenite-inhibited, NADH-reduced LipDH; (b) FAD catalytic activity in a NADH-nitrofuran model system; and (c) the nitroreductase activity of LipDH monomer. Two-electron nitrofuran reduction to less oxidized products was inhibited by cadmium, arsenite and NAD+. The possible role of reactive nitrosofuran derivatives as intermediates of the nitrofuran reduction sequence was supported by the LipDH capability for catalysing 2-nitroso-1-naphthol redox-cycling. The nitroso naphthol reduction was inhibited by cadmium and arsenite, like the two-electron nitrofuran reduction.
为阐明硝基呋喃生物活化的机制，研究了这些化合物与硫辛酰胺脱氢酶（LipDH）** 的相互作用。LipDH催化了几种硝基呋喃衍生物的单电子还原反应。该反应可用光谱法证明，且镉、亚砷酸盐和缺氧条件可增强此反应。黄素在硝基还原酶活性中的作用得到以下几点支持：（a）硝基呋喃对厌氧、亚砷酸盐抑制、NADH还原的LipDH光谱特性的影响；（b）FAD在NADH-硝基呋喃模型系统中的催化活性；（c）LipDH单体的硝基还原酶活性。镉、亚砷酸盐和NAD + 抑制了硝基呋喃向氧化程度较低产物的双电子还原反应。LipDH催化2-亚硝基-1-萘酚氧化还原循环的能力支持了活性亚硝基呋喃衍生物作为硝基呋喃还原序列中间体的可能作用。亚硝基萘酚的还原反应与双电子硝基呋喃还原反应一样，受到镉和亚砷酸盐的抑制。
