Fujiwara K, Sato H, Bannai S
Department of Biochemistry, Institute of Basic Medical Sciences, University of Tsukuba, Ibaraki, Japan.
FEBS Lett. 1998 Jul 10;431(1):116-20. doi: 10.1016/s0014-5793(98)00735-2.
Oxidation of low-density lipoprotein (LDL) can be mediated in vitro by cultured cells, including macrophages. This cellular oxidation is dependent on the production of free thiols by the cells in the presence of transition metal ions. We now report that the production of thiols by macrophages is greatly enhanced when cells are cultured with lipopolysaccharide (LPS) or tumor necrosis factor-alpha (TNF-alpha). Oxidation of LDL by macrophages is markedly augmented by pre-treatment of the cells with LPS or TNF-alpha. The results suggest that activation by endotoxins or TNF-alpha is a necessary step for macrophages to mediate oxidation of LDL.
低密度脂蛋白（LDL）的氧化在体外可由包括巨噬细胞在内的培养细胞介导。这种细胞氧化取决于细胞在过渡金属离子存在下产生的游离硫醇。我们现在报告，当巨噬细胞与脂多糖（LPS）或肿瘤坏死因子-α（TNF-α）一起培养时，硫醇的产生会大大增强。用LPS或TNF-α预处理细胞后，巨噬细胞对LDL的氧化会显著增强。结果表明，内毒素或TNF-α的激活是巨噬细胞介导LDL氧化的必要步骤。
