Gavino V C, Miller J S, Ikharebha S O, Milo G E, Cornwell D G
J Lipid Res. 1981 Jul;22(5):763-9.
Lipid peroxidation was measured by the thio-barbituric assay for malondialdehyde (MDA). A small amount of MDA was formed when medial cells from guinea pig aorta were grown in tissue culture. The polyunsaturated fatty acids 8,11,14-eicosatrienoic acid, 5,8,11,14-eicosatetraenoic acid, and 7,10,13,16-docosatetraenoic acid generated significant amounts of MDA in a time-dependent manner when they were added to cultures of medial cells and fibroblasts. MDA or its precursor remained within the cell and did not accumulate in the media. Indomethacin enhanced MDA formation from polyunsaturated fatty acid. Alpha-Tocopherol, alpha-tocopherolquinone, and 2,6-di-tert-butyl-4-methylphenol (BHT) inhibited MDA formation when a polyunsaturated fatty acid was incubated with the pro-oxidant cumene hydroperoxide. Menadione had no effect on MDA formation in the cumene hydroperoxide system. Alpha-Tocopherol and alpha-tocopherolquinone inhibited MDA formation when they were added to cells in culture. Menadione had no effect on MDA formation in tissue culture. Anti-oxidant effects which were time-dependent showed that intracellular MDA was generated from a lipid peroxide precursor during the thiobarbituric acid assay. Relative plating efficiency was measured in medial cells and fibroblasts. Alpha-Tocopherolquinone and alpha-tocopherol enhanced the extent of cell proliferation. Alpha-Tocopherolquinone overcame the inhibitory effect of a polyunsaturated fatty acid on the extent of cell proliferation. Menadione was cytotoxic. Thus antioxidant data support the hypothesis that the extent of cell proliferation is controlled in part by lipid peroxidation.
通过硫代巴比妥酸法测定丙二醛(MDA)来检测脂质过氧化。当豚鼠主动脉中层细胞在组织培养中生长时,会形成少量的MDA。当将多不饱和脂肪酸8,11,14-二十碳三烯酸、5,8,11,14-二十碳四烯酸和7,10,13,16-二十二碳四烯酸添加到中层细胞和成纤维细胞培养物中时,它们会以时间依赖性方式产生大量的MDA。MDA或其前体保留在细胞内,不会在培养基中积累。吲哚美辛可增强多不饱和脂肪酸生成MDA的过程。当多不饱和脂肪酸与促氧化剂氢过氧化异丙苯一起孵育时,α-生育酚、α-生育醌和2,6-二叔丁基-4-甲基苯酚(BHT)可抑制MDA的形成。甲萘醌在氢过氧化异丙苯系统中对MDA的形成没有影响。当α-生育酚和α-生育醌添加到培养的细胞中时,它们可抑制MDA的形成。甲萘醌在组织培养中对MDA的形成没有影响。抗氧化作用具有时间依赖性,表明在硫代巴比妥酸测定过程中,细胞内的MDA是由脂质过氧化物前体产生的。在中层细胞和成纤维细胞中测量相对铺板效率。α-生育醌和α-生育酚可提高细胞增殖程度。α-生育醌克服了多不饱和脂肪酸对细胞增殖程度的抑制作用。甲萘醌具有细胞毒性。因此,抗氧化数据支持细胞增殖程度部分受脂质过氧化控制这一假说。