Wenzel D C, Hale T W
Toxicology. 1978 Oct;11(2):119-25. doi: 10.1016/s0300-483x(78)90839-9.
Oleic (C18:1), linoleic (C18:2), linolenic (C18:3) and arachidonic (C20:4) acids were compared for their toxic effects upon cultured rat heart muscle and endothelioid cells. The free fatty acids (FFA) were bound to albumin (6:1) and tested at concentrations from 5 x 10(-5)M to 5 x 10(-4)M. Reduction of cell viability (51Cr release) and in situ mitochondrial and lysosomal labilization were used as indices of injury. Oleic acids was non-toxic at all times and concentrations tested while linoleic acid increased cell death only in muscle cells after 32 h. Arachidonic acid, by contrast, demonstrated significant toxicity as early as 2 h while both linolenic and arachidonic acids produced major injury at longer durations. A detergent effect was excluded as the injury mechanism because of marked differences in the toxicities of the individual FFA. The similarity in the effects of linolenic and arachidonic acids would appear to exclude prostaglandins as responsible toxic products.
比较了油酸（C18:1）、亚油酸（C18:2）、亚麻酸（C18:3）和花生四烯酸（C20:4）对培养的大鼠心肌细胞和内皮样细胞的毒性作用。游离脂肪酸（FFA）与白蛋白以6:1的比例结合，并在5×10⁻⁵M至5×10⁻⁴M的浓度下进行测试。以细胞活力降低（⁵¹Cr释放）以及原位线粒体和溶酶体的不稳定作为损伤指标。在所测试的所有时间和浓度下，油酸均无毒，而亚油酸仅在32小时后才增加肌肉细胞的死亡。相比之下，花生四烯酸早在2小时就表现出显著毒性，而亚麻酸和花生四烯酸在较长时间后都会造成严重损伤。由于各游离脂肪酸的毒性存在显著差异，排除了去污剂效应作为损伤机制。亚麻酸和花生四烯酸作用的相似性似乎排除了前列腺素作为有毒产物的可能性。
