A review of animal model studies of tomato carotenoids, lycopene, and cancer chemoprevention
A review of animal model studies of tomato carotenoids, lycopene, and cancer chemoprevention
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DOI：
10.1177/153537020222701005
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发表时间：
2002-11-01
影响因子：
3.2
通讯作者：
Cohen, LA
中科院分区：
文献类型：
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作者：
Cohen, LA
关于番茄红素或番茄类胡萝卜素在动物模型中的癌症化学预防作用的报道相对较少。这些研究中的大多数（但不是全部）都表明具有保护作用。两项使用异常隐窝病灶（一种导致结肠癌的中间病变）作为终点的研究和两项乳腺肿瘤研究报告了抑制作用，一项使用二甲基苯并（a）蒽模型，另一项使用自发小鼠模型。在小鼠肺癌、大鼠肝癌和膀胱癌模型中也报告了抑制作用。然而，作者实验室的一份报告发现，在饮食中添加结晶番茄红素或富含番茄红素的番茄类胡萝卜素油树脂时，对 N-亚硝基甲基脲诱导的乳腺肿瘤模型没有影响。不幸的是，由于给药途径（强饲、腹腔注射、直肠内滴注、饮用水和饮食补充剂）、物种和菌株差异、番茄红素形式（纯晶体、微珠、混合类胡萝卜素悬浮液）、不同饮食（基于谷物、基于酪蛋白）和剂量范围（0.5-500 ppm）的差异，没有两项研究具有可比性。很明显，大部分摄入的番茄红素通过粪便排出，肝脏中吸收和储存的番茄红素比其他靶器官中积累的番茄红素多 1000 倍。尽管如此，生理上显着（纳克）水平的番茄红素会被乳腺、前列腺、肺和结肠等关键器官吸收，并且番茄红素摄入量和血液水平之间存在粗略的剂量反应关系。纯番茄红素的吸收效率低于富含番茄红素的番茄类胡萝卜素油树脂，并且以谷物为基础的饮食喂养的大鼠中番茄红素的血液水平始终低于以酪蛋白为基础的饮食中喂养番茄红素的大鼠。后者表明，番茄红素掺入的基质是番茄红素吸收的重要决定因素。在就番茄红素的抗癌作用得出任何明确结论之前，仍有许多问题需要解决。这些包括以下内容：番茄红素的最佳剂量和形式、番茄红素与其他类胡萝卜素和脂溶性维生素（如维生素 E 和 D）之间的相互作用、膳食脂肪在调节番茄红素吸收和分布中的作用、器官和组织特异性，以及从啮齿动物模型外推到人类群体的问题。
There are relatively few reports on the cancer chemopreventive effects of lycopene or tomato carotenoids in animal models. The majority, but not all, of these studies indicate a protective effect. Inhibitory effects were reported in two studies using aberrant crypt foci, an intermediate lesion leading to colon cancer, as an end point and in two mammary tumor studies, one using the dimethylbenz(a)anthracene model, and the other the spontaneous mouse model. Inhibitory effects were also reported in mouse lung and rat hepatocarcinoma and bladder cancer models. However, a report from the author's laboratory found no effect in the N-nitrosomethylurea-induced mammary tumor model when crystalline lycopene or a lycopene-rich tomato carotenoid oleoresin was administered in the diet. Unfortunately, because of differences in routes of administration (gavage, intraperitoneal injection, intra-rectal instillation, drinking water, and diet supplementation), species and strain differences, form of lycopene (pure crystalline, beadlet, mixed carotenoid suspension), varying diets (grain-based, casein based) and dose ranges (0.5-500 ppm), no two studies are comparable. It is clear that the majority of ingested lycopene is excreted in the feces and that 1000-fold more lycopene is absorbed and stored in the liver than accumulates in other target organs. Nonetheless, physiologically significant (nanogram) levels of lycopene are assimilated by key organs such as breast, prostate, lung, and colon, and there is a rough dose-response relationship between lycopene intake and blood levels. Pure lycopene was absorbed less efficiently than the lycopene-rich tomato carotenoid oleoresin and blood levels of lycopene in rats fed a grain-based diet were consistently lower than those in rats fed lycopene in a casein-based diet. The latter suggests that the matrix in which lycopene is incorporated is an important determinant of lycopene uptake. A number of issues remain to be resolved before any definitive conclusions can be drawn concerning the anticancer effects of lycopene. These include the following: the optimal dose and form of lycopene, interactions among lycopene and other carotenoids and fat soluble vitamins such as vitamin E and D, the role of dietary fat in regulating lycopene uptake and disposition, organ and tissue specificity, and the problem of extrapolation from rodent models to human populations.