Fernandez Y, Subirade I, Anglade F, Periquet A, Mitjavila S
Laboratoire des Xénobiotiques, INRA, Toulouse, France.
Biol Trace Elem Res. 1995 Jan-Mar;47(1-3):9-15. doi: 10.1007/BF02790096.
Descriptions of the effects of paraquat (P2+) on the peroxidation of liver microsomes are very divergent. Therefore, the presence of ferric iron in the medium and the activity of microsomal mixed-function oxidase system are two factors that we have taken into consideration to explain the discrepancies. The results showed that 100 microM P2+ potentializes the slight production of MDA induced by low concentrations of Fe3+ (< or = 15 microM). In these conditions, P+., arising from the one-step reduction of P2+ by NADPH-cytochrome C reductase, could reduce Fe3+ and cause the formation of species that initiate peroxidation. However, unlike the results obtained with CBrCl3, for animals induced by phenobarbital (Ph), the production of MDA in the presence of FeCl3 and of P2+ was weaker than for the controls. The establishment of a new Fe3+/Fe2+ equilibrium owing to increased production of P+. could be responsible.
关于百草枯(P2+)对肝微粒体过氧化作用的描述差异很大。因此,培养基中三价铁的存在以及微粒体混合功能氧化酶系统的活性是我们为解释这些差异而考虑的两个因素。结果表明,100微摩尔/升的P2+增强了低浓度Fe3+(≤15微摩尔/升)诱导的丙二醛的轻微生成。在这些条件下,由NADPH-细胞色素C还原酶将P2+一步还原产生的P+.可还原Fe3+并导致引发过氧化的物质形成。然而,与用三氯溴甲烷得到的结果不同,对于苯巴比妥(Ph)诱导的动物,在存在FeCl3和P2+的情况下丙二醛的生成比对照组弱。由于P+.生成增加导致新的Fe3+/Fe2+平衡的建立可能是其原因。