Ishida-Okawara A, Tsuchiya T, Nunoi H, Mizuno S, Suzuki K
Department of Bioactive Molecules, National Institute of Health, Tokyo, Japan.
Biochim Biophys Acta. 1996 Dec 12;1314(3):239-46. doi: 10.1016/s0167-4889(96)00110-3.
Unsaturated fatty acids of odd carbons, 13:1(12), 17:1(10trans), 19:1(7) and 19:1(10) inhibited release of myeloperoxidase (MPO) from fMet-Leu-Phe-cytochalasin B-treated neutrophils. The inhibitory effect was smaller than that of aseanostatins which have been isolated as microbial-derived free fatty acids with a methyl blanch (i-14:0 and ai-15:0) (Journal of Antibiotics (1991) 44, 524-532). These unsaturated fatty acids also inhibited lactoferrin release by the same treatment. On the other hand, 13:1(12), 15:1(10) and 19:1(10) inhibited fMet-Leu-Phe-stimulated superoxide generation of neutrophils, and the fatty acids 15:1(10), 17:(10) and 19:2(10,13) induced superoxide generation in both unstimulated cells and the cell-free system. However, none of unsaturated fatty acids of odd carbons tested inhibited beta-glucuronidase release, whereas 15:1(10), 17:1(10), 19:1(10) and 19:2(10,13) rather enhanced an increase in beta-glucuronidase activity liberated from cells at high concentrations over 35 microM, indicating cellular damages by these fatty acids. These observations suggest that unsaturated free fatty acids having odd carbons such as 13, 15, 17 and 19 may act as modulators of neutrophil functions including degranulation and superoxide generation.
奇数碳不饱和脂肪酸，13:1(12)、17:1(10反式)、19:1(7)和19:1(10)，抑制了甲酰甲硫氨酰-亮氨酰-苯丙氨酸-细胞松弛素B处理的中性粒细胞中髓过氧化物酶（MPO）的释放。其抑制作用小于已作为具有甲基支链的微生物衍生游离脂肪酸（i-14:0和ai-15:0）分离得到的阿西诺他汀（《抗生素杂志》（1991年）44卷，524 - 532页）。这些不饱和脂肪酸通过相同处理也抑制了乳铁蛋白的释放。另一方面，13:1(12)、15:1(10)和19:1(10)抑制了甲酰甲硫氨酰-亮氨酰-苯丙氨酸刺激的中性粒细胞超氧化物生成，并且脂肪酸15:1(10)、17:(10)和19:2(10,13)在未刺激细胞和无细胞体系中均诱导了超氧化物生成。然而，所测试的奇数碳不饱和脂肪酸均未抑制β-葡萄糖醛酸酶的释放，而15:1(10)、17:1(10)、19:1(10)和19:2(10,13)在浓度超过35微摩尔时反而增强了从细胞中释放的β-葡萄糖醛酸酶活性的增加，表明这些脂肪酸对细胞造成了损伤。这些观察结果表明，具有13、15、17和19等奇数碳的不饱和游离脂肪酸可能作为中性粒细胞功能（包括脱颗粒和超氧化物生成）的调节剂。
