Robinson K M, Botha J H
Prostaglandins Leukot Med. 1985 Nov;20(2):209-21. doi: 10.1016/0262-1746(85)90011-3.
A number of fatty acids have been shown to inhibit the growth of malignant cells in vitro. In particular, gamma-linolenic acid (GLA) has been proposed to act as a precursor for the production of prostanoids especially prostaglandin E1 (PGE1). To test this hypothesis, the effects of GLA on cultured human breast carcinoma cells were compared with those of dihomo-gamma-linolenic acid (DGLA) the metabolite of GLA and the immediate precursor of PGE1. The influence of ethanol (which has been shown to enhance conversion of DGLA to PGE1) on the actions of each of the fatty acids was also investigated. In contrast to the inhibitory effects observed with all concentrations of GLA cell growth was promoted by the presence of 50 micrograms DGLA. Ethanol reduced the action of both GLA and DGLA possibly due to some physicochemical reaction between the alcohol and the fatty acids. The fact that the actions of GLA were not mimicked by DGLA which is the next step towards PG production casts doubt upon the role of PGE1 as mediator of the effects which have been observed with GLA in malignant cells.
许多脂肪酸已被证明在体外可抑制恶性细胞的生长。特别是，γ-亚麻酸（GLA）被认为是前列腺素尤其是前列腺素E1（PGE1）生成的前体。为了验证这一假设，将GLA对培养的人乳腺癌细胞的作用与二高-γ-亚麻酸（DGLA，GLA的代谢产物及PGE1的直接前体）的作用进行了比较。还研究了乙醇（已证明可增强DGLA向PGE1的转化）对每种脂肪酸作用的影响。与所有浓度的GLA所观察到的抑制作用相反，50微克DGLA的存在促进了细胞生长。乙醇可能由于酒精与脂肪酸之间的某种物理化学反应而降低了GLA和DGLA的作用。DGLA作为PG生成的下一步，其作用并未模拟GLA的作用，这一事实使人对PGE1作为在恶性细胞中观察到的GLA效应的介质的作用产生怀疑。
