Wainberg R H, Walden T L, Stebler B A, Yatvin M B
Biology Department, Piedmont College, Demorest, GA 30531.
Prostaglandins. 1991 May;41(5):501-13. doi: 10.1016/0090-6980(91)90056-l.
Hyperthermia-induced cell lethality is thought to be mediated through injury to the cell membrane. Membrane perturbation results in the release of prostaglandins (PG) and leukotrienes (LT). These compounds are potent biological mediators and may modify the tumor microenvironment and therapeutic efficacy. Membrane composition and PG/LT release are influenced by the dietary fatty acids. The relationship between these variables and response to hyperthermia was examined in vitro using murine P388 leukemia cells grown as an ascites in mice provided either saturated fatty acid diet (SFA; 16% beef tallow) or unsaturated fatty acid diet (UFA; 16% safflower oil). Cells were harvested and exposed in vitro to either 37 degrees C or 43.5 degrees C for periods up to 2 hours. Hyperthermic exposure for 2 hours resulted in 40% cell lethality in SFA cells and 55% in UFA cells. The phospholipid and total cholesterol content was higher (33% and 50% respectively) in the UFA versus the SFA cells. Hyperthermia produced a six-fold increase in prostaglandin E2 PGE2 release by SFA cells and a 4.5-fold increase by UFA cells. No LTC4 was detected. Alteration of dietary fat affects cell lethality and PG release following hyperthermic treatment. The increase in phospholipid and cholesterol content of UFA cells may be a response to reduced membrane fluidity.
热疗诱导的细胞致死性被认为是通过对细胞膜的损伤介导的。膜扰动导致前列腺素(PG)和白三烯(LT)的释放。这些化合物是强效的生物介质,可能会改变肿瘤微环境和治疗效果。膜组成以及PG/LT释放受膳食脂肪酸的影响。使用在给予饱和脂肪酸饮食(SFA;16%牛脂)或不饱和脂肪酸饮食(UFA;16%红花油)的小鼠体内以腹水形式生长的小鼠P388白血病细胞,在体外研究了这些变量与热疗反应之间的关系。收获细胞并在体外分别于37℃或43.5℃暴露长达2小时。热疗暴露2小时导致SFA细胞中40%的细胞致死率,UFA细胞中55%的细胞致死率。与SFA细胞相比,UFA细胞中的磷脂和总胆固醇含量更高(分别为33%和50%)。热疗使SFA细胞的前列腺素E2(PGE2)释放增加了6倍,UFA细胞增加了4.5倍。未检测到LTC4。改变膳食脂肪会影响热疗后的细胞致死率和PG释放。UFA细胞中磷脂和胆固醇含量的增加可能是对膜流动性降低的一种反应。