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膳食纤维对二甲肼诱导的Wistar大鼠异常隐窝病灶发展及结肠癌发生率的影响。

Influence of a dietary fiber on development of dimethylhydrazine-induced aberrant crypt foci and colon tumor incidence in Wistar rats.

作者信息

Thorup I, Meyer O, Kristiansen E

机构信息

Institute of Toxicology, National Food Agency, Søborg, Denmark.

出版信息

Nutr Cancer. 1994;21(2):177-82. doi: 10.1080/01635589409514315.

DOI:10.1080/01635589409514315
PMID:8058528
Abstract

Formation of aberrant crypt foci (ACF) in archived colon tissue from animals in a previous study was examined. The animals were fed a semisynthetic casein-based diet in which the carbohydrate pool was substituted with a dietary beet fiber (Fibeta) as the only source of fiber. Oral doses of dimethylhydrazine dihydrochloride (DMH-2HCl, 20 mg/kg body wt) once a week for 10 weeks were used as initiator. The rats were fed different levels of the fiber in a preinitiation period, during initiation, or in a postinitiation period. In general, the results showed a statistically significant inverse relation between duration of intake of high-fiber diet and number of animals with ACF, as well as the total number of ACF and number of small ACF (1-3 crypts) per affected animal. The previously reported data showed no protective effect of the dietary fiber at any stage of the colorectal carcinogenic process. The lack of correlation between the outcome of ACF and tumors could be related to the observation that statistically significant differences between groups were seen only in the total number of ACF and number of small ACF. The hypothesis that ACF are preneoplastic lesions needs to be supported by further experimental data. The present state of knowledge could indicate that ACF represent true preneoplastic lesions progressing into colon tumors or that ACF and colon tumors represent two parallel independent events as a consequence of the cancer initiation (i.e., the ACF not being preneoplastic lesions per se).

摘要

对先前一项研究中动物存档结肠组织中异常隐窝灶(ACF)的形成进行了检查。给动物喂食一种半合成的酪蛋白基饮食,其中碳水化合物库被膳食甜菜纤维(Fibeta)替代,作为唯一的纤维来源。每周口服一次二盐酸二甲肼(DMH - 2HCl,20 mg/kg体重),持续10周作为启动剂。在启动前、启动期间或启动后,给大鼠喂食不同水平的纤维。总体而言,结果显示高纤维饮食摄入持续时间与出现ACF的动物数量、ACF总数以及每只受影响动物的小ACF(1 - 3个隐窝)数量之间存在统计学上显著的负相关。先前报道的数据表明膳食纤维在结直肠癌致癌过程的任何阶段均无保护作用。ACF结果与肿瘤之间缺乏相关性可能与以下观察结果有关:仅在ACF总数和小ACF数量上观察到组间存在统计学上的显著差异。ACF是癌前病变这一假说需要进一步的实验数据支持。目前的知识状况可能表明,ACF代表真正进展为结肠肿瘤的癌前病变,或者ACF和结肠肿瘤代表癌症启动后的两个平行独立事件(即ACF本身不是癌前病变)。

相似文献

1
Influence of a dietary fiber on development of dimethylhydrazine-induced aberrant crypt foci and colon tumor incidence in Wistar rats.膳食纤维对二甲肼诱导的Wistar大鼠异常隐窝病灶发展及结肠癌发生率的影响。
Nutr Cancer. 1994;21(2):177-82. doi: 10.1080/01635589409514315.
2
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Nutr Cancer. 1995;23(2):151-9. doi: 10.1080/01635589509514371.
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Effect of a dietary fiber (beet fiber) on dimethylhydrazine-induced colon cancer in Wistar rats.膳食纤维(甜菜纤维)对二甲基肼诱导的Wistar大鼠结肠癌的影响。
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The incidence of aberrant crypt foci and colonic carcinoma in dimethylhydrazine-treated rats varies in a site-specific manner and depends on tumor histology.二甲基肼处理的大鼠中异常隐窝灶和结肠癌的发生率因部位而异,并取决于肿瘤组织学类型。
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Effect of dietary cellulose on cell proliferation and progression of 1,2-dimethylhydrazine-induced colon carcinogenesis in rats.膳食纤维素对1,2 - 二甲基肼诱导的大鼠结肠癌发生过程中细胞增殖及进展的影响
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Modulation of experimental colon tumorigenesis by types and amounts of dietary fatty acids.膳食脂肪酸的类型和数量对实验性结肠肿瘤发生的调节作用。
Cancer Res. 2001 Mar 1;61(5):1927-33.

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Development and distribution of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced aberrant crypt foci in the rat large intestine.
2-氨基-1-甲基-6-苯基咪唑并[4,5-b]吡啶(PhIP)诱导的大鼠大肠异常隐窝病灶的发生与分布
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Ingestion of sugar beet fiber enhances irradiation-induced aberrant crypt foci in the rat colon under an apoptosis-suppressed condition.在细胞凋亡受到抑制的情况下,摄入甜菜纤维会增加大鼠结肠中辐射诱导的异常隐窝病灶。
Carcinogenesis. 1999 Jun;20(6):1005-9. doi: 10.1093/carcin/20.6.1005.
5
Development of aberrant crypt foci involves a fission mechanism as revealed by isolation of aberrant crypts.异常隐窝病灶的形成涉及一种裂变机制,这是通过分离异常隐窝所揭示的。
Jpn J Cancer Res. 1996 Dec;87(12):1199-203. doi: 10.1111/j.1349-7006.1996.tb03133.x.
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Distribution of lymphoid nodules, aberrant crypt foci and tumours in the colon of carcinogen-treated rats.
Br J Cancer. 1996 Apr;73(7):893-8. doi: 10.1038/bjc.1996.159.