Lewin M R, Ferulano G P, Cruse J P, Clark C G
Carcinogenesis. 1981;2(12):1363-6. doi: 10.1093/carcin/2.12.1363.
The theory that endogenous factors in the intestinal contents may be pathogenic during large bowel carcinogenesis was tested in the dimethylhydrazine (DMH)-induced rat colon cancer model. Thirty female Wistar rats, each serving as their own control, had a surgical transection of the proximal colon with reanastomosis to the rectum, thereby excluding part of the colon from faecal contact. All rats then received a course of DMH (40 mg/kg body wt/wk s.c. for 10 weeks) while fed on Vivonex. This diet was selected because it lacks known exogenous (dietary) cocarcinogens. It also produces mucosal atrophy in functioning (proximal) colon, to parallel the disuse atrophy induced in the defunctioned (distal) colon. Animals remained on the diet throughout the experiment and were killed when moribund or at 40 weeks. At necropsy, the anatomical distribution, number, size and histological type of colon tumours were compared between functioning and defunctioned colonic segments within the same animal. At autopsy, there were significantly fewer colon tumours in the defunctioned segment (P less than 0.005). Furthermore, there were significantly fewer carcinomas (P less than 0.005) and fewer tumours greater than 1 cm diameter (P less than 0.01) in this segment. The data indicate that endogenous factors in the intestinal contents facilitate chemically-induced colon carcinogenesis. Luminal nutrition may be implicated.
在二甲基肼（DMH）诱导的大鼠结肠癌模型中，对肠道内容物中的内源性因素在大肠癌发生过程中可能具有致病性这一理论进行了验证。30只雌性Wistar大鼠，每只大鼠自身作为对照，接受近端结肠手术横断并与直肠重新吻合，从而使部分结肠不与粪便接触。然后所有大鼠在喂食Vivonex的同时接受一个疗程的DMH（40mg/kg体重/周，皮下注射，共10周）。选择这种饮食是因为它缺乏已知的外源性（饮食中的）促癌剂。它还会使有功能的（近端）结肠产生黏膜萎缩，以与无功能的（远端）结肠中诱导产生的废用性萎缩相平行。动物在整个实验过程中一直食用这种饮食，在濒死时或40周时处死。尸检时，比较同一动物中有功能和无功能结肠段之间结肠肿瘤的解剖分布、数量、大小和组织学类型。尸检时，无功能段的结肠肿瘤明显较少（P<0.005）。此外，该段的癌明显较少（P<0.005），直径大于1cm的肿瘤也较少（P<0.01）。数据表明，肠道内容物中的内源性因素促进化学诱导的结肠癌发生。管腔营养可能与之有关。
