Wright J R, Colby H D, Miles P R
Biochim Biophys Acta. 1980 Aug 11;619(2):374-84. doi: 10.1016/0005-2760(80)90085-5.
The effects of substances known to influence lipid peroxidation were studied in guinea pig lung microsomes by measuring the formation of malonaldehyde in vitro. Incubation of lung microsomes at 37 degrees C results in lipid peroxidation which appears to be an enzymatic process but is not dependent upon iron. Lipid peroxidation can be initiated non-enzymatically in lung microsomes by Fe2+, but ascorbate and Fe3+ have very little effect on malonaldehyde formation. The effects of NADPH on lipid peroxidation are dependent upon the concentration of Fe2+ in the incubation medium. At concentrations of Fe2+ between 0.05 mM and 1 mM, addition of NADPH causes an increase in lipid peroxidation over that produced by Fe2+ alone. This stimulation by NADPH is an enzymatic process and phosphate is required for the maximal effect. Addition of NADPH to lung microsomes in the presence of Fe3+ does not increase malonaldehyde formation over that produced by Fe3+ alone, suggesting that NADPH does not influence lipid peroxidation by maintaining iron in the reduced form. At concentrations of Fe2+ greater than 1 mM, NADPH inhibits Fe2+-induced lipid peroxidation in normal microsomes and in microsomes in which enzymes have been inactivated with heat. This latter result suggests that the inhibition by NADPH is at least partially non-enzymatic. The result suggests that the inhibition by NADPH is at least partially non-enzymatic. The results of all of these experiments are discussed and compared with those obtained during lipid peroxidation in liver microsomes. We conclude that the processes involved in pulmonary microsomal lipid peroxidation differ significantly from those in hepatic microsomes.
通过体外测量丙二醛的生成,研究了已知影响脂质过氧化的物质对豚鼠肺微粒体的作用。在37摄氏度孵育肺微粒体会导致脂质过氧化,这似乎是一个酶促过程,但不依赖于铁。脂质过氧化可由Fe2+在肺微粒体中非酶促引发,但抗坏血酸和Fe3+对丙二醛的生成影响很小。NADPH对脂质过氧化的影响取决于孵育介质中Fe2+的浓度。在Fe2+浓度为0.05 mM至1 mM之间时,添加NADPH会导致脂质过氧化比单独由Fe2+产生的增加。NADPH的这种刺激是一个酶促过程,最大效应需要磷酸盐。在Fe3+存在下向肺微粒体中添加NADPH不会使丙二醛生成比单独由Fe3+产生的增加,这表明NADPH不会通过将铁维持在还原形式来影响脂质过氧化。在Fe2+浓度大于1 mM时,NADPH抑制正常微粒体和酶已被热灭活的微粒体中Fe2+诱导的脂质过氧化。后一个结果表明NADPH的抑制至少部分是非酶促的。结果表明NADPH的抑制至少部分是非酶促的。讨论了所有这些实验的结果,并与在肝微粒体脂质过氧化过程中获得的结果进行了比较。我们得出结论,肺微粒体脂质过氧化所涉及的过程与肝微粒体中的过程有显著差异。