Vitamin E inhibits the high-fat diet promoted growth of established human prostate LNCaP tumors in nude mice
Vitamin E inhibits the high-fat diet promoted growth of established human prostate LNCaP tumors in nude mice
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DOI：
10.1016/s0022-5347(05)68998-7
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发表时间：
1999-05-01
影响因子：
6.6
通讯作者：
Heston, WDW
中科院分区：
文献类型：
--
作者：
Fleshner, N;Fair, WR;Heston, WDW
目的：前列腺癌已成为西方世界一个重要的公共卫生问题。它是目前最常见的诊断癌症，也是北美男性癌症死亡的第二大原因。前列腺癌具有独特的描述性流行病学，这表明环境因素（如膳食脂肪消耗）在肿瘤进展中起着关键作用。来自我们机构的数据表明，高脂肪含量的饮食可以加速人类LNCaP前列腺癌细胞的生长。膳食脂肪诱导生长的假设机制之一是氧化应激。我们的目的是确定补充维生素E，一种有效的细胞内抗氧化剂，对高脂肪促进的移植LNCaP细胞生长的无胸腺muse.Materials和方法的效果：通过皮下注射10（6）LNCaP细胞诱导肿瘤。给小鼠喂食由来自膳食脂肪的总热量的40.5%组成的对照饮食。一旦肿瘤形成，获得PSA值，并将动物随机分为4组，每组12只。然后将动物分配至4个饮食计划之一。第1组接受40.5%千卡脂肪的对照饮食。第2组接受40.5%大卡脂肪饮食加补充维生素E。第3组接受21.2%千卡脂肪的饮食。第4组给予21.2%-kcal脂肪饲料加补充维生素E。每周记录摄食量、动物体重和肿瘤体积。生存率分析，目标体积为0.523 cm。(3)（定义为失败）用于比较4组之间的肿瘤生长。结果：在喂食40.5%千卡脂肪饮食的动物中肿瘤生长率最高（p < 0.05，第1组）。喂食40.5%千卡脂肪加维生素E、21.2%千卡脂肪和21.2%千卡脂肪加维生素E的动物中的肿瘤经历了统计学上不可区分的生长速率。没有显着差异，注意到在总摄入的热量，动物体重增加或初始PSA levels.Conclusions：这些数据表明，膳食脂肪诱导人前列腺癌细胞生长的机制是由氧化应激介导的。它还提高了维生素E在预防前列腺癌方面的治疗益处的可能性。
Purpose: Prostate cancer has become an important public health problem in the Western world. It is currently the most common diagnosed cancer and the second leading cause of cancer deaths among North American men. Prostate cancer possesses a unique descriptive epidemiology which suggests that environmental factors (such as dietary fat consumption) play a pivotal role in tumor progression. Data from our institution have demonstrated that diets high in fat content can accelerate the growth of human LNCaP prostate cancer cells. One of the hypothesized mechanisms of dietary fat induced growth is oxidative stress. Our purpose was to determine the effect of supplemental Vitamin E, a potent intracellular antioxidant, on the high-fat promoted growth of transplanted LNCaP cells in the athymic mouse.Materials and Methods: Tumors were induced by subcutaneous injection of 10(6) LNCaP cells. Mice were fed a control diet consisting of 40.5% of total calories from dietary fat. Once tumors were formed, PSA values were obtained and animals were randomized into 4 groups of 12. The animals were then assigned to one of 4 dietary plans. Group 1 received the control diet of 40.5%-kcal fat. Group 2 received the 40.5%-kcal fat diet plus supplemental Vitamin E. Group 3 received a diet of 21.2%-kcal fat. Group 4 received the 21.2%-kcal fat diet plus supplemental Vitamin E. Food intake, animal weights, and, tumor volumes were recorded weekly. Survival analyses with time to a target volume of 0.523 cm.(3) (defined as failure) were used to compare tumor growth among the 4 groups. Two-sided tests (log rank test) with a set at 0.05 were used to determine significance.Results: tumor growth rates were highest in the animals fed a 40.5%-kcal fat diet (p < 0.05 group 1). Tumors in animals fed 40.5%-kcal fat plus Vitamin E, 21.2%-kcal fat, and 21.2%-kcal fat plus Vitamin E, experienced statistically indistinguishable growth rates. No significant differences were noted in total ingested calories, animal weight gain or initial PSA levels.Conclusions: These data suggest that the mechanism of dietary fat induced growth of human prostate cancer cells is mediated by oxidative stress. It also raises the possibility of a therapeutic benefit of vitamin E in preventing prostate cancer.