Healy Declan A, Watson R William G, Newsholme Philip
Department of Biochemistry, University College Dublin, Belfield, Dublin 4, Ireland.
Clin Sci (Lond). 2003 Feb;104(2):171-9. doi: 10.1042/CS20020223.
We report here that monounsaturated fatty acids and polyunsaturated fatty acids (PUFAs) provoke the accumulation of neutral lipids and apoptosis in retinoic acid-treated HL-60 cells in a concentration- and time-dependent manner. The PUFAs (arachidonic acid, docosahexanoic acid and eicosapentaenoic acid) provoked higher levels of HL-60 apoptosis compared with the monounsaturated oleic acid or the saturated palmitic acid. Cell size and granularity were also altered by fatty acid treatment. The PUFA-induced apoptosis was correlated with increased activity of caspase 3 and caspase 9. Lipid peroxidation was also increased in the presence of PUFAs, but was not responsible for activating cell apoptosis. Lipid derived metabolites may be responsible for activation of caspases and induction of cell apoptosis.
我们在此报告,单不饱和脂肪酸和多不饱和脂肪酸(PUFAs)以浓度和时间依赖性方式促使视黄酸处理的HL-60细胞中中性脂质积累和细胞凋亡。与单不饱和油酸或饱和棕榈酸相比,PUFAs(花生四烯酸、二十二碳六烯酸和二十碳五烯酸)引发的HL-60细胞凋亡水平更高。脂肪酸处理还改变了细胞大小和粒度。PUFA诱导的细胞凋亡与caspase 3和caspase 9活性增加相关。在PUFAs存在的情况下,脂质过氧化也增加,但这并非激活细胞凋亡的原因。脂质衍生代谢产物可能是激活caspases和诱导细胞凋亡的原因。