了解葡萄酒与癌症关系的动物模型和分析方法。

S E Ebeler, K H Dingley, E Ubick, S Abel, A E Mitchell, S A Burns, F M Steinberg, A J Clifford
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摘要

我们使用了两种方法来研究葡萄酒消费、葡萄酒成分与癌症之间的关系。第一种方法是用人类神经纤维瘤病的转基因小鼠模型,结合使用定义明确的、化学纯化的饮食,表明红酒含有可以延缓肿瘤发作的非酒精成分。在进一步的研究中,儿茶素,红酒中的主要单体多酚,在小鼠模型中以0.5-4 mmol/kg的水平加入饮食时,呈正线性关系延迟肿瘤的发生。在第二种方法中,给大鼠低剂量的化学致癌物质2-氨基-1-甲基-6-苯基咪唑(4,5 -b)吡啶(PhlP),并通过加速器质谱法评估DNA加合物的形成。饮用红酒固体(红酒去除酒精和水后残留的残留物)和红酒多酚槲皮素不会影响php - dna加合物水平,也不会诱导肝酶(谷胱甘肽- s转移酶和醌还原酶)。然而,与对照动物和喂食其他潜在的化学预防剂(包括异硫氰酸苯乙基酯和萝卜硫素)的动物相比,槲皮素确实改变了PhlP在大鼠组织中的分布。这些研究证明了这些方法在生理水平上研究膳食成分的化学预防潜力的可行性
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Animal models and analytical approaches for understanding the relationships between wine and cancer.

We used two approaches for studying the relationships between wine consumption, wine composition and cancer In the first approach, a transgenic mouse model of human neurofibromatosis, combined with the use of well-defined, chemically purified diets, showed that red wine contains nonalcoholic components that can delay tumor onset. In additional studies, catechin, the main monomeric polyphenol of red wine, delayed tumor onset in this mouse model in a positive, linear relationship when incorporated into the diet at levels of 0.5-4 mmol/kg diet. In the second approach, low doses of the chemical carcinogen 2-amino-1-methyl-6-phenylimidazo(4, 5-b)pyridine (PhlP) were administered to rats, and formation of DNA adducts was evaluated by accelerator mass spectrometry. Consumption of red wine solids (the residue from red wine remaining after removal of alcohol and water) and the wine polyphenol quercetin did not influence PhlP-DNA adduct levels or induce liver enzymes (glutathione-S-transferase and quinone reductase). However, quercetin did alter distribution of PhlP in the rat tissues compared to control animals and animals fed other potential dietary chemopreventive agents, including phenylethyl isothiocyanate and sulforaphane. These studies demonstrate the feasibility of these approaches for studying the chemopreventive potential of dietary components at physiologic levels in

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