Nenseter M S, Halvorsen B, Rosvold O, Rustan A C, Drevon C A
Institute for Nutrition Research, University of Oslo, Norway.
Arterioscler Thromb Vasc Biol. 1995 Sep;15(9):1338-44. doi: 10.1161/01.atv.15.9.1338.
The effects of paracetamol and sodium salicylate on the susceptibility of LDL to oxidative modification were studied. LDL was subjected to Cu(2+)-, azo compound-, or peripheral blood mononuclear cell-initiated oxidation in the absence and presence of paracetamol and salicylate. Paracetamol (100 mumol/L; 25 micrograms LDL/mL) reduced the rate of formation of conjugated dienes and the amount of conjugated dienes formed during Cu(2+)-induced oxidation by 67% and 58%, respectively. Paracetamol (400 mumol/L; 100 micrograms LDL/mL) reduced the generation of lipid peroxides during Cu(2+)-induced oxidation by 43% (P < .05), the relative electrophoretic mobility in agarose gels by 16% (P < .05), and the amount of oxidized LDL taken up by J774 macrophages by 22% (P < .05). Paracetamol (100 mumol/L; 100 micrograms LDL/mL) reduced the 2,2'-azobis-(2-amidinopropane hydrochloride)-initiated lipid peroxidation by 70% (P < .05) and the relative electrophoretic mobility by 34% (P < .05). Paracetamol (100 mumol/L; 100 micrograms LDL/mL) reduced the amount of lipid peroxides generated in LDL during mononuclear cell-mediated oxidation by 69% (P < .01) and the relative electrophoretic mobility by 38% (P < .01). In comparison, 10 mumol/L alpha-tocopherol reduced the amount of lipid peroxides formed during cellular LDL oxidation and the relative electrophoretic mobility by 52% and 65%, respectively (P < .05). In the absence of paracetamol, SOD and catalase inhibited the modification of LDL (P < .05), suggesting that superoxide anions and hydrogen peroxide might be involved in the cell-mediated modification pathway. In the presence of paracetamol, SOD showed no additional inhibitory effect.(ABSTRACT TRUNCATED AT 250 WORDS)
研究了对乙酰氨基酚和水杨酸钠对低密度脂蛋白（LDL）氧化修饰敏感性的影响。在有无对乙酰氨基酚和水杨酸盐的情况下，使LDL受到铜离子（Cu(2+)）、偶氮化合物或外周血单核细胞引发的氧化作用。对乙酰氨基酚（100 μmol/L；每毫升LDL含25微克）使共轭二烯的形成速率以及在Cu(2+)诱导氧化过程中形成的共轭二烯量分别降低了67%和58%。对乙酰氨基酚（400 μmol/L；每毫升LDL含100微克）使Cu(2+)诱导氧化过程中脂质过氧化物的生成量降低了43%（P < 0.05），琼脂糖凝胶中的相对电泳迁移率降低了16%（P < 0.05），J774巨噬细胞摄取的氧化LDL量降低了22%（P < 0.05）。对乙酰氨基酚（100 μmol/L；每毫升LDL含100微克）使2,2'-偶氮双（2-脒基丙烷盐酸盐）引发的脂质过氧化作用降低了70%（P < 0.05），相对电泳迁移率降低了34%（P < 0.05）。对乙酰氨基酚（100 μmol/L；每毫升LDL含100微克）使单核细胞介导的氧化过程中LDL产生的脂质过氧化物量降低了69%（P < 0.01），相对电泳迁移率降低了38%（P < 0.01）。相比之下，10 μmol/L的α-生育酚使细胞内LDL氧化过程中形成的脂质过氧化物量和相对电泳迁移率分别降低了52%和65%（P < 0.05）。在无对乙酰氨基酚的情况下，超氧化物歧化酶（SOD）和过氧化氢酶抑制了LDL的修饰（P < 0.05），这表明超氧阴离子和过氧化氢可能参与了细胞介导的修饰途径。在有对乙酰氨基酚存在的情况下，SOD没有显示出额外的抑制作用。（摘要截短至250字）
