Das U N, Begin M E, Ells G, Huang Y S, Horrobin D F
Biochem Biophys Res Commun. 1987 May 29;145(1):15-24. doi: 10.1016/0006-291x(87)91281-2.
Polyunsaturated fatty acids (PUFAs) have been shown to inhibit both normal and tumor cell growth in vitro. As PUFAs are known to induce a respiratory burst and free radical generation in polymorphonuclear leukocytes and since free radicals are toxic to cells, we investigated the effect of PUFAs on a measure of free radical generation (nitroblue tetrazolium reduction) in normal human fibroblasts and breast cancer cells in vitro. Results suggested that linoleate (LA), gamma-linolenate (GLA), arachidonate (AA) and eicosapentaenoate (EPA) can enhance nitroblue tetrazolium reduction in tumor cells but not in normal cells. GLA, AA and EPA were 1 1/2 to 2 times more effective than LA in inducing free radical generation. This difference was not due to increased uptake of LA, AA and EPA by tumor cells. In fact, the uptake of LA was the same both in normal and tumor cells whereas that of AA and EPA occurred at approximately half the rate in the tumor cells compared to normal cells. This indicates that PUFA induced growth inhibition and cytotoxicity to tumor cells may, at least in part, be due to enhanced free radical generation.
多不饱和脂肪酸（PUFAs）已被证明在体外可抑制正常细胞和肿瘤细胞的生长。由于已知PUFAs会在多形核白细胞中诱导呼吸爆发和自由基生成，且自由基对细胞有毒性，因此我们研究了PUFAs对正常人成纤维细胞和乳腺癌细胞体外自由基生成指标（硝基蓝四氮唑还原）的影响。结果表明，亚油酸（LA）、γ-亚麻酸（GLA）、花生四烯酸（AA）和二十碳五烯酸（EPA）可增强肿瘤细胞中的硝基蓝四氮唑还原，但对正常细胞无此作用。在诱导自由基生成方面，GLA、AA和EPA的效果比亚油酸强1.5至2倍。这种差异并非由于肿瘤细胞对LA、AA和EPA的摄取增加。事实上，正常细胞和肿瘤细胞对LA的摄取相同，而与正常细胞相比，肿瘤细胞对AA和EPA的摄取速率约为正常细胞的一半。这表明PUFAs诱导的肿瘤细胞生长抑制和细胞毒性可能至少部分归因于自由基生成的增强。
