Brogan W C, Miles P R, Colby H D
Environ Health Perspect. 1981 Apr;38:105-10. doi: 10.1289/ehp.8138105.
Studies were carried out to determine the actions of and interactions between ascorbate, NADPH, Fe2+, and Fe3+ on lipid peroxidation in adrenal and testicular microsomes. Ascorbate-induced malonaldehyde production was maximal in adrenal and testicular microsomes at an ascorbate concentration of 1 X 10(-4)M. Fe2+, at levels between 10(-6) and 10(-3)M, produced concentration-dependent increases in lipid peroxidation in adrenal and testicular microsomes; Fe2+ had a far greater effect than Fe3+ in both tissues. In liver microsomes, by contrast, Fe2+ and Fe3+ had quantitatively similar effects on lipid peroxidation. NADPH alone had no effect on malonaldehyde production in adrenal or testicular microsomes. However, in the presence of low Fe2+ concentrations (10(-6)M), NADPH stimulated adrenal malonaldehyde production. The stimulation of lipid peroxidation by NADPH plus low Fe2+ was not demonstrable in testicular microsomes nor in adrenal microsomes which had been heat-treated to inactivate microsomal enzymes. Testicular malonaldehyde production was stimulated by NADPH if Fe3+ (5 X 10(-5) to 1 X 10(-3)M) was added to the incubation medium; the stimulation was not demonstrable in heat-treated microsomes. Fe3+ plus NADPH had little effect on adrenal lipid peroxidation. In the presence of high Fe2+ levels (10(-3)M), NADPH produced a concentration-dependent inhibition of adrenal lipid peroxidation; the inhibition was fully demonstrable in heat-treated microsomes. NADPH similarly inhibited ascorbate-induced lipid peroxidation in adrenal microsomes. In testicular microsomes, NADPH did not inhibit ascorbate or Fe2+-induced lipid peroxidation. The results indicate that various endogenous substances may be important in the control of adrenal and testicular lipid peroxidation and that the nature of the regulation differs from tissue to tissue.
开展了多项研究，以确定抗坏血酸盐、NADPH、Fe2+和Fe3+对肾上腺和睾丸微粒体脂质过氧化的作用及它们之间的相互作用。在抗坏血酸盐浓度为1×10(-4)M时，肾上腺和睾丸微粒体中抗坏血酸盐诱导的丙二醛生成量达到最大值。Fe2+浓度在10(-6)至10(-3)M之间时，肾上腺和睾丸微粒体中的脂质过氧化呈浓度依赖性增加；在这两种组织中，Fe2+的作用远比Fe3+大。相比之下，在肝微粒体中，Fe2+和Fe3+对脂质过氧化的作用在数量上相似。单独的NADPH对肾上腺或睾丸微粒体中的丙二醛生成没有影响。然而，在低Fe2+浓度（10(-6)M）存在的情况下，NADPH会刺激肾上腺丙二醛的生成。NADPH加低Fe2+对脂质过氧化的刺激在睾丸微粒体中以及经过热处理使微粒体酶失活的肾上腺微粒体中均未得到证实。如果在孵育培养基中加入Fe3+（5×10(-5)至1×10(-3)M），NADPH会刺激睾丸丙二醛的生成；在经过热处理的微粒体中未观察到这种刺激作用。Fe3+加NADPH对肾上腺脂质过氧化的影响很小。在高Fe2+水平（10(-3)M）存在的情况下，NADPH会对肾上腺脂质过氧化产生浓度依赖性抑制；这种抑制在经过热处理的微粒体中完全可以观察到。NADPH同样抑制肾上腺微粒体中抗坏血酸盐诱导的脂质过氧化。在睾丸微粒体中，NADPH不抑制抗坏血酸盐或Fe2+诱导的脂质过氧化。结果表明，各种内源性物质可能在肾上腺和睾丸脂质过氧化的控制中起重要作用，并且调节的性质因组织而异。
