Lack of influence of low blood cholesterol levels on pancreatic carcinogenesis after initiation with N-nitrosobis(2-oxopropyl)amine in Syrian golden hamsters.

Lack of influence of low blood cholesterol levels on pancreatic carcinogenesis after initiation with N-nitrosobis(2-oxopropyl)amine in Syrian golden hamsters.
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叙利亚金仓鼠开始使用 N-亚硝基双(2-氧代丙基)胺后,低血液胆固醇水平对胰腺癌的发生缺乏影响。

DOI:
10.1093/carcin/15.8.1663
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发表时间:
1994
期刊:
影响因子:
4.7
通讯作者:
M. Sugano
M. Sugano
中科院分区:
医学2区
文献类型:
--
作者:
T. Ogawa;T. Makino;N. Hirose;M. Sugano

文献摘要

被引文献

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在140只雌性叙利亚金黄仓鼠中研究了无胆固醇饮食、无胆固醇饮食添加芝麻素和饮食添加芝麻素对N-亚硝基双(2-氧代丙基)胺(BOP)胰腺癌发生的影响。将BOP(70和20 mg/kg体重)s.c.实验开始时每隔2周进行两次。此后3周开始,动物继续接受基础饮食、无胆固醇饮食、基础饮食加芝麻素或无胆固醇饮食加芝麻素维持15周。第18周处死所有存活仓鼠,并对胰腺组织进行组织学检查。各组中胰腺肿瘤和癌前病变的发生率未显示任何统计学显著性变化。无胆固醇饮食显著降低血清、胰腺和肝脏的胆固醇含量,芝麻素补充显著降低血清和肝脏的胆固醇含量。无胆固醇饮食和芝麻素都能降低血清过氧化脂质水平。因此,结果表明,低胆固醇本身和芝麻素对BOP引发的仓鼠胰腺癌发生没有显着影响,至少在致癌剂治疗后的4个月内。
The effects of a cholesterol-free diet, a cholesterol-free diet supplemented with sesamin, and a diet supplemented with sesamin on pancreatic carcinogenesis of N-nitrosobis(2-oxopropyl)amine (BOP) were investigated in 140 female Syrian golden hamsters. BOP (70 and 20 mg/kg body wt) was injected s.c. twice at an interval of 2 weeks at the beginning of the experiment. Starting 3 weeks thereafter, the animals were maintained on basal diet, cholesterol-free diet, basal diet plus sesamin, or cholesterol-free diet plus sesamin for a further 15 weeks. All surviving hamsters were killed at week 18, and the pancreatic tissues examined histologically. The incidences of pancreatic neoplastic and preneoplastic lesions in each group did not show any statistically significant variation. The cholesterol-free diet significantly decreased the cholesterol contents of the serum, pancreas and liver, and sesamin supplement significantly decreased the cholesterol contents of the serum and liver. Both the cholesterol-free diet and sesamin decreased the serum lipoperoxide levels. The results thus indicated that low cholesterol per se and sesamin exert no significant influence on BOP-initiated pancreatic carcinogenesis in hamsters, at least within the 4 month period after carcinogen treatment.