Cope R B, Loehr C, Dashwood R, Kerkvliet N I
Photochem Photobiol Sci. 2006 May;5(5):499-507. doi: 10.1039/b515556h. Epub 2006 Apr 7.
Over 1 million new cases of ultraviolet radiation-induced non-melanoma skin cancers (NMSC) per year now occur in the USA and the incidence of these diseases continues to increase. New preventative strategies are required. The hypothesis tested was that dietary administration of the putative cancer chemopreventatives sodium-copper-chlorophyllin (Chlor) or indole-3-carbinol (I3C) would inhibit UV-induced skin carcinogenesis in the Crl:SKH1:hr-BR hairless mouse. Groups of 20 mice were pre-fed isocaloric/isonutritive 20% corn-oil AIN-76a based diets that contained either Chlor (1.52 g%), I3C (5.08 g%) or no chemopreventative (control) for 2 weeks followed by exposure of their dorsal skin to a 10 week incremental, sub-erythemal, carcinogenic simulated solar UV exposure regime. Feeding was continued for the duration of the experiment. Matched non-UV exposed dietary groups were also included in the experimental design. The diets had no significant (p > 0.05) effect on body weight, feed consumption, cutaneous methanol-extractable UV photoprotective substances or on cutaneous UV-reflective characteristics. By day 180, UV-irradiated mice fed the Chlor had a significantly (p < 0.05) higher tumor multiplicity (33.6 +/- 4.72; mean +/- SEM) than UV-irradiated control animals (22.8 +/- 4.25). UV-irradiated mice fed I3C had a significantly (p < 0.001) lower tumor multiplicity (13.0 +/- 2.42) than that of both the UV-irradiated control and UV-irradiated Chlor-fed mice. The Chlor or I3C diets did not significantly (p > 0.05) affect UV-induced systemic suppression of contact hypersensitivity responses. These results demonstrate augmentation of the UV-induced cutaneous carcinogenic process by dietary chlorophyllin and protection from this carcinogenic process by indole-3-carbinol via mechanisms that do not involve changes in skin optical properties, modulation of photoimmunosuppression or caloric/nutrient effects.
目前，美国每年新增超过100万例紫外线辐射诱发的非黑素瘤皮肤癌（NMSC），且这些疾病的发病率持续上升。需要新的预防策略。本研究检验的假设是，在饮食中给予假定的癌症化学预防剂叶绿素铜钠盐（Chlor）或吲哚 - 3 - 甲醇（I3C），将抑制Crl:SKH1:hr - BR无毛小鼠的紫外线诱导的皮肤癌发生。将20只小鼠分为几组，预先喂食基于20%玉米油AIN - 76a的等热量/等营养饮食，其中一组饮食含有Chlor（1.52 g%），另一组含有I3C（5.08 g%），第三组不含有化学预防剂（对照组），持续2周，随后将它们的背部皮肤暴露于为期10周的递增、亚红斑、致癌性模拟太阳紫外线照射方案。在整个实验过程中持续喂食。实验设计中还包括了未接受紫外线照射的匹配饮食组。这些饮食对体重、饲料消耗、皮肤甲醇可提取的紫外线光保护物质或皮肤紫外线反射特性均无显著（p > 0.05）影响。到第180天时，喂食Chlor的紫外线照射小鼠的肿瘤多发性显著（p < 0.05）高于紫外线照射的对照动物（分别为33.6 ± 4.72和22.8 ± 4.25；均值 ± 标准误）。喂食I3C的紫外线照射小鼠的肿瘤多发性显著（p < 0.001）低于紫外线照射的对照小鼠和喂食Chlor的紫外线照射小鼠（为13.0 ± 2.42）。Chlor或I3C饮食对紫外线诱导的接触性超敏反应的全身抑制作用无显著（p > 0.05）影响。这些结果表明，饮食中的叶绿素铜钠盐增强了紫外线诱导的皮肤致癌过程，而吲哚 - 3 - 甲醇通过不涉及皮肤光学性质变化、光免疫抑制调节或热量/营养效应的机制，对这一致癌过程具有保护作用。
