Locniskar M, Belury M A, Cumberland A G, Patrick K E, Fischer S M
Division of Nutrition, University of Texas, Austin 78712.
Carcinogenesis. 1990 Sep;11(9):1641-5. doi: 10.1093/carcin/11.9.1641.
Fish oil has been shown to have a protective effect in some cancer models. To determine whether fish oil alters skin tumorigenesis, a study was designed using the initiation-promotion mouse skin carcinogenesis model, feeding mice during the promotion stage a constant overall amount of dietary fat (10%) in which the levels of menhaden oil (MO) varied from 0 to 8.5% or corn oil (CO) at 10%. SENCAR mice were initiated with 10 nmol dimethylbenz[a]anthracene. Two weeks later mice were divided into five groups and maintained on one of the following AIN-76 based diets consisting of: 8.5% coconut oil (CT)/1.5% CO (diet A); 1% MO/7.5% CT/1.5% CO (diet B); 4% MO/4.5% CT/1.5% CO (diet C); 8.5% MO/1.5% CO (diet D); or 10% CO (diet E). Two weeks later, promotion with twice weekly applications of 1 micrograms 12-O-tetradecanoylphorbol-13-acetate (TPA) was begun and continued for 24 weeks. No statistically significant differences in kcal food consumed or body wts were observed between diet groups during the study. The final papilloma and carcinoma incidence was not different among the diet groups. However, differences were seen in the rate of papilloma appearance with the group fed diet E (10% CO) being the slowest and diet B being the most rapid. In a parallel study, ornithine decarboxylase activity, a suggested marker of promotion, was greatly elevated in the epidermis of all TPA-treated mice and the effect of diet tended to reflect the different rates of tumor formation observed among the groups. These data indicate that the diets containing fish oil were not protective in the final incidence of tumor formation and suggest that a better understanding of the complex interactions is warranted before recommendations are made to alter the human diet for cancer prevention.
鱼油已被证明在某些癌症模型中具有保护作用。为了确定鱼油是否会改变皮肤肿瘤发生过程，研究人员设计了一项研究，采用启动-促癌小鼠皮肤癌发生模型，在促癌阶段给小鼠喂食总脂肪含量恒定为10%的饮食，其中鲱鱼油（MO）水平从0变化到8.5%，或玉米油（CO）含量为10%。用10 nmol二甲基苯并[a]蒽启动SENCAR小鼠。两周后，将小鼠分为五组，并维持在以下基于AIN-76的饮食之一上，这些饮食包括：8.5%椰子油（CT）/1.5% CO（饮食A）；1% MO/7.5% CT/1.5% CO（饮食B）；4% MO/4.5% CT/1.5% CO（饮食C）；8.5% MO/1.5% CO（饮食D）；或10% CO（饮食E）。两周后，开始每周两次涂抹1微克12-O-十四烷酰佛波醇-13-乙酸酯（TPA）进行促癌，持续24周。在研究期间，各饮食组之间在消耗的千卡食物量或体重方面未观察到统计学上的显著差异。各饮食组之间最终的乳头状瘤和癌发病率没有差异。然而，在乳头状瘤出现的速率上存在差异，喂食饮食E（10% CO）的组最慢，饮食B的组最快。在一项平行研究中，鸟氨酸脱羧酶活性是一种提示促癌的标志物，在所有经TPA处理的小鼠表皮中均大幅升高，饮食的影响倾向于反映各组中观察到的不同肿瘤形成速率。这些数据表明，含鱼油的饮食对肿瘤形成的最终发病率没有保护作用，并表明在就改变人类饮食以预防癌症提出建议之前，有必要更好地理解复杂的相互作用。
