Lipotrope deficiency in experimental carcinogenesis
Lipotrope deficiency in experimental carcinogenesis
复制标题
实验性致癌作用中的抗脂肽缺乏
DOI：
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发表时间：
1980
期刊：
影响因子：
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通讯作者：
P. Newberne
中科院分区：
文献类型：
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作者：
A. E. Rogers;P. Newberne
缺乏抗脂蛋白（蛋氨酸、胆碱和叶酸）和高脂肪的饮食会增加许多化学物质引起的肝癌，包括黄曲霉毒素B1（AFB1）和N-2-芴基乙酰胺（AAF）。在大多数情况下，这种增加可以通过补充抗脂素来纠正，但纠正的程度似乎受到饮食中脂肪类型的影响。缺乏促脂素的高脂肪饮食也会增加结肠中二甲肼的致癌作用，这是由于饮食中的脂肪含量而不是促脂素缺乏引起的。相比之下，乳腺癌的二甲基苯并芘或AAF减少或不变的大鼠喂养的缺陷饮食。在体外试验中，使用脂溶性缺乏大鼠的组织，肝微粒体氧化酶活性、细胞色素P450和AFB 1转化为细菌诱变剂均降低。然而，尿诱变剂含量增加AFB1治疗后，是尿中的含量激活AAF。体内AFB1与肝DNA的结合没有变化或略有下降。t...
Abstract Diets deficient in lipotropes (methionine, choline, and folate) and high in fat increase hepatocarcinogenesis by many chemicals, including aflatoxin B1 (AFB1) and N‐2‐fluor‐enylacetamide (AAF). The increase can be corrected in most cases by lipotrope supplementation, but the degree of correction appears to be influenced by the type of fat in the diet. A lipotrope‐deficient, high‐fat diet also increases dimethylhydrazine carcinogenesis in the colon, an effect due to the dietary fat content, not to lipotrope deficiency. In contrast, mammary carcinogenesis by dimethylbenzanthrene or AAF is decreased or unchanged in rats fed the deficient diet. Hepatic microsomal oxidase activity, cytochrome P450 and conversion of AFB 1 to a bacterial mutagen all are decreased in assays in vitro using tissues from lipotrope‐deficient rats. However, urine mutagen content is increased after AFB1 treatment, as is urine content of activated AAF. AFB1 binding to hepatic DNA in vivo is unchanged or is slightly decreased. T...