Locniskar M, Belury M A, Cumberland A G, Patrick K E, Fischer S M
Division of Nutrition, University of Texas, Austin 78712.
Carcinogenesis. 1991 Jun;12(6):1023-8. doi: 10.1093/carcin/12.6.1023.
Fish or vegetable oils were fed during the promotion stage of a mouse skin carcinogenesis model in order to investigate the effects of dietary fat on tumor development. Two weeks after initiation with 10 nmol dimethylbenz[a]anthracene, SENCAR mice were divided into five groups and maintained on one of the following semipurified diets containing 10% total fat and varying the type of fat: 8.5% coconut oil (CT)/1.5% corn oil (CO); 1% menhaden oil (MO)/7.5% CT/1.5% CO; 4% MO/4.5% CT/1.5% CO; 8.5% MO/1.5% CO; or 10% CO. Promotion with twice-weekly applications of 40 mg benzoyl peroxide was begun 2 weeks later and continued for 52 weeks. No statistically significant differences in kcal food consumed or body weights were observed between diet groups. Papilloma latency, incidence and yield differed among the diet groups with the group fed the 8.5% CT/1.5% CO diet having the shortest latency and highest papilloma incidence and number. In addition, carcinoma latency and incidence was assessed and the first carcinoma appeared in the group fed 8.5% CT/1.5% CO after 20 weeks of benzoyl peroxide treatment; this group yielded the highest carcinoma incidence throughout the study. In comparison, the group fed the 10% CO diet had the longest latency period, and among the lowest papilloma and carcinoma incidence and fewest tumors. In parallel studies, ornithine decarboxylase activity, vascular permeability and hyperplasia were elevated in the epidermis of benzoyl peroxide-treated mice but the extent of the response did not correlate with the different rates of tumor formation observed among the diet groups. These data indicate that dietary fat modulates tumor promotion by benzoyl peroxide in this skin carcinogenesis model with the predominantly saturated fat diet producing the highest rates of papilloma and carcinogen formation and the polyunsaturated fat diet the lowest.
在小鼠皮肤癌发生模型的促进阶段喂食鱼油或植物油，以研究膳食脂肪对肿瘤发展的影响。用10 nmol二甲基苯并[a]蒽启动实验两周后，将SENCAR小鼠分为五组，并维持在以下含10%总脂肪且脂肪类型不同的半纯化饮食之一上：8.5%椰子油（CT）/1.5%玉米油（CO）；1%鲱鱼油（MO）/7.5%CT/1.5%CO；4%MO/4.5%CT/1.5%CO；8.5%MO/1.5%CO；或10%CO。两周后开始每周两次涂抹40 mg过氧化苯甲酰进行促进，持续52周。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。饮食组之间的乳头瘤潜伏期、发生率和产量有所不同，喂食8.5%CT/1.5%CO饮食的组潜伏期最短，乳头瘤发生率和数量最高。此外，评估了癌的潜伏期和发生率，在过氧化苯甲酰处理20周后，喂食8.5%CT/1.5%CO的组出现了首例癌；在整个研究中，该组的癌发生率最高。相比之下，喂食10%CO饮食的组潜伏期最长，乳头瘤和癌的发生率最低，肿瘤数量最少。在平行研究中，过氧化苯甲酰处理的小鼠表皮中的鸟氨酸脱羧酶活性、血管通透性和增生增加，但反应程度与饮食组中观察到的不同肿瘤形成率无关。这些数据表明，在这个皮肤癌发生模型中，膳食脂肪调节过氧化苯甲酰的肿瘤促进作用，主要含饱和脂肪的饮食产生最高的乳头瘤和致癌物形成率，而多不饱和脂肪饮食产生的率最低。
