Dubin M, Grinblat L, Fernandez Villamil S H, Stoppani A O
FEBS Lett. 1987 Aug 10;220(1):197-200. doi: 10.1016/0014-5793(87)80902-x.
Two nitrofuran compounds, nifurtimox and nitrofurantoin, inhibited in a concentration-dependent manner the NADPH-, iron-induced lipid peroxidation in rat liver microsomes, as shown by the decreased rate of MDA accumulation. Other nitro compounds (benznidazole and chloramphenicol) were relatively inactive. Nifurtimox inhibition affected polyenoic fatty acids and cytochrome P-450 degradation that follows lipid peroxidation. The ascorbate- or tert-butyl hydroperoxide-dependent lipid peroxidations were much less inhibited than the NADPH-dependent one. Nifurtimox and nitrofurantoin, but not benznidazole and chloramphenicol, strongly stimulated the microsomal NADPH-oxidase activity, thus supporting electron diversion, as the main cause of the inhibition of peroxidation initiation.
两种硝基呋喃化合物,硝呋替莫和呋喃妥因,以浓度依赖性方式抑制大鼠肝微粒体中NADPH-铁诱导的脂质过氧化,丙二醛积累速率降低表明了这一点。其他硝基化合物(苯硝唑和氯霉素)相对无活性。硝呋替莫的抑制作用影响了多不饱和脂肪酸和脂质过氧化后细胞色素P-450的降解。抗坏血酸或叔丁基过氧化氢依赖性脂质过氧化受到的抑制远小于NADPH依赖性脂质过氧化。硝呋替莫和呋喃妥因,而非苯硝唑和氯霉素,强烈刺激微粒体NADPH氧化酶活性,从而支持电子转移,作为过氧化起始抑制的主要原因。