Woutersen R A, van Garderen-Hoetmer A, Bax J, Feringa A W, Scherer E
Carcinogenesis. 1986 Sep;7(9):1587-93. doi: 10.1093/carcin/7.9.1587.
The effect of dietary fat and ethanol and their interactions on the development of putative, preneoplastic foci in exocrine pancreas was investigated in rats and hamsters. Rats were given a single i.p. injection of 30 mg azaserine per kg body wt at 19 days of age. Hamsters were injected s.c., with 20 mg N-nitrosobis(2-oxopropyl)amine (BOP)/kg body wt at 6 and 7 weeks of age. The animals were fed a low fat (LF) control diet (5% corn oil) or a high fat (HF) diet (25% corn oil). Ethanol was provided in drinking water at a 15% (w/v) concentration. The animals were given the respective diets and ethanol after the treatment with carcinogen. At 4 months post-initiation, the pancreata were quantitatively examined for the number and size of preneoplastic foci. In rats, acidophilic as well as basophilic foci were subject to modulation by HF and ethanol. The results point to a specific promoting effect of unsaturated fat on the growth potential of azaserine-induced acidophilic acinar cell foci in rat pancreas. There was no evidence of an interaction between HF and ethanol as far as acidophilic foci are concerned. Evaluation of the number and size of the basophilic foci demonstrated an enhancing effect of ethanol on the modulation of pancreatic carcinogenesis by fat, pointing to a possible interaction between these two lifestyle factors. This suggestion was supported by the finding that six out of 20 rats in the HF with ethanol group exhibited a carcinoma in situ, whereas in the HF and in the ethanol group such an advanced lesion was found in one animal only. Unlike in rats, ethanol had no modulating effect on number and growth of putative, preneoplastic lesions in hamsters, either in combination with LF or in combination with HF. A HF diet, however, caused a significant increase in number as well as an increase in percentage of pancreatic tissue occupied by early lesions induced in hamster pancreas by BOP.
在大鼠和仓鼠中研究了膳食脂肪和乙醇及其相互作用对外分泌胰腺中假定的癌前病灶发展的影响。大鼠在19日龄时腹腔注射每千克体重30毫克的重氮丝氨酸。仓鼠在6周和7周龄时皮下注射每千克体重20毫克的N-亚硝基双(2-氧代丙基)胺(BOP)。动物被喂食低脂(LF)对照饮食(5%玉米油)或高脂(HF)饮食(25%玉米油)。饮用水中乙醇的浓度为15%(w/v)。动物在接受致癌物处理后给予相应的饮食和乙醇。在启动后4个月,对胰腺进行定量检查,以确定癌前病灶的数量和大小。在大鼠中,嗜酸性和嗜碱性病灶都受到高脂饮食和乙醇的调节。结果表明不饱和脂肪对大鼠胰腺中重氮丝氨酸诱导的嗜酸性腺泡细胞病灶的生长潜力具有特定的促进作用。就嗜酸性病灶而言,没有证据表明高脂饮食和乙醇之间存在相互作用。对嗜碱性病灶数量和大小的评估表明,乙醇对脂肪调节胰腺癌发生具有增强作用,表明这两种生活方式因素之间可能存在相互作用。这一观点得到了以下发现的支持:高脂饮食加乙醇组的20只大鼠中有6只出现原位癌,而在高脂饮食组和乙醇组中,只有1只动物出现这种晚期病变。与大鼠不同,乙醇对仓鼠中假定的癌前病变的数量和生长没有调节作用,无论是与低脂饮食还是高脂饮食组合。然而,高脂饮食导致仓鼠胰腺中由BOP诱导的早期病变的数量显著增加,以及胰腺组织被占据的百分比增加。