Kuroiwa Yuichi, Ishii Yuji, Umemura Takashi, Kanki Keita, Mitsumori Kunitoshi, Nishikawa Akiyoshi, Nakazawa Hiroyuki, Hirose Masao
Division of Pathology, National Institute of Health Sciences, Tokyo 158-8501, Japan.
Cancer Sci. 2007 Jul;98(7):949-57. doi: 10.1111/j.1349-7006.2007.00481.x. Epub 2007 Apr 12.
Combined treatment with several phenolic antioxidants and sodium nitrite (NaNO(2)) has already shown to enhance rat forestomach carcinogenesis. In the present experiment, effects of green tea catechins (GTC) alone or in combination with NaNO(2) on gastric carcinogenesis were investigated in a rat two-stage carcinogenesis model. Groups of eight, 6-week-old F344 male rats were given 0.01%N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in their drinking water and 5% NaCl in the diet for 10 weeks for glandular stomach initiation and a single intragastric administration of 100 mg/kg/bodyweight of MNNG at week 9 for forestomach initiation. From week 11, they received either drinking water containing 0.2% NaNO(2) and a diet supplemented with 1% GTC in combination, each individual chemical alone or a basal diet until the end of week 42. In the forestomach, incidences and multiplicities of neoplastic lesions were clearly increased by the combined treatment, in spite of GTC alone suppressing the occurrence of papillomas. In a short-term experiment with similar protocol without MNNG pretreatment, a significant increase of 8-hydroxydeoxyguanosine (8-OHdG) levels in forestomach DNA occurred 24 h after the combined treatment, concomitant with erosion and inflammatory cell infiltration. In an in vitro study, electron spin resonance demonstrated hydroxyl radical formation after incubation of epigallocatechin gallate or epicatechin gallate with the NO generator, NOC-7. Thus, GTC alone showed a weak chemopreventive effect on forestomach carcinogenesis, but in the presence of NaNO(2) it exerted a promotive effect which might involve hydroxyl-radical-associated oxidative DNA damage. However, no influence was exerted in the glandular stomach.
几种酚类抗氧化剂与亚硝酸钠(NaNO₂)联合治疗已显示会增强大鼠前胃癌变。在本实验中,在大鼠两阶段癌变模型中研究了单独使用绿茶儿茶素(GTC)或与NaNO₂联合使用对胃癌变的影响。将八组6周龄的F344雄性大鼠,在其饮用水中给予0.01%的N-甲基-N'-硝基-N-亚硝基胍(MNNG),在饮食中给予5%的NaCl,持续10周以启动腺胃癌变,并在第9周单次胃内给予100 mg/kg体重的MNNG以启动前胃癌变。从第11周开始,它们接受含有0.2% NaNO₂的饮用水和添加1% GTC的组合饮食、每种单独的化学物质或基础饮食,直至第42周结束。在前胃中,联合治疗明显增加了肿瘤性病变的发生率和多发性,尽管单独使用GTC可抑制乳头状瘤的发生。在一个没有MNNG预处理的类似方案的短期实验中,联合治疗24小时后前胃DNA中的8-羟基脱氧鸟苷(8-OHdG)水平显著增加,同时伴有糜烂和炎性细胞浸润。在一项体外研究中,电子自旋共振显示表没食子儿茶素没食子酸酯或儿茶素没食子酸酯与NO发生器NOC-7孵育后会形成羟基自由基。因此,单独使用GTC对前胃癌变显示出较弱的化学预防作用,但在存在NaNO₂的情况下,它发挥了促进作用,这可能涉及与羟基自由基相关的氧化性DNA损伤。然而,在腺胃中未产生影响。