Birt D F
Proc Soc Exp Biol Med. 1986 Dec;183(3):311-20. doi: 10.3181/00379727-183-42424.
The effects of vitamins A, C, and E and of selenium on carcinogenesis are briefly summarized and updated. These vitamins and minerals were selected because they have been studied extensively in recent years with a variety of carcinogenesis models. The consumption of vitamin A and its precursors (carotenoids) has been negatively correlated with cancer at a number of sites, particularly the lung. Animal investigations on vitamin A involvement in carcinogenesis have generally been of three types: those assessing the effect of vitamin A deficiency, the effect of excess vitamin A, or the effect of supplementation with synthetic analogs of vitamin A. Vitamin A deficiency had no effect on salivary gland carcinogenesis, enhanced urinary bladder, lung, and liver carcinogenesis, and inhibited colon carcinogenesis. Excess of various forms of vitamin A enhanced or inhibited skin tumorigenesis, inhibited mammary carcinogenesis in rats (but not in mice), and carcinogenesis of the forestomach, liver, and urinary bladder (with one model, but not with another), or enhanced or did not influence lung carcinogenesis. Vitamin A analogs have enhanced or inhibited skin tumorigenesis, inhibited salivary gland, mammary, and urinary bladder carcinogenesis, enhanced tracheal and liver carcinogenesis, and either enhanced or inhibited pancreas carcinogenesis, depending upon the model employed. Although retinoids have been shown to inhibit carcinogenesis at many sites, numerous negative studies have been reported and some reports have indicated enhanced carcinogenesis. The most convincing evidence for the involvement of vitamin C in cancer prevention is the ability of ascorbic acid to prevent formation of nitrosamine and of other N-nitroso compounds. In addition vitamin C supplementation was shown to inhibit skin, nose, tracheal, lung, and kidney carcinogenesis, to either not influence or enhance skin, mammary gland, and colon carcinogenesis, and to enhance urinary bladder carcinogenesis, when given as sodium ascorbate, but not when given as ascorbic acid. Like vitamin C, vitamin E can inhibit nitrosation. Vitamin E was shown to inhibit skin, cheek pouch, and forestomach carcinogenesis, to enhance or inhibit colon carcinogenesis, and to have no effect on or to inhibit mammary gland carcinogenesis, depending upon the method of vitamin E administration or the level of dietary selenium or dietary fat. Selenium effects on carcinogenesis have been recently reviewed and the present discussion only updates this area by indicating that enhancement of carcinogenesis by dietary selenium supplements has been observed in the liver, pancreas, and skin.(ABSTRACT TRUNCATED AT 400 WORDS)
简要总结并更新了维生素A、C、E以及硒对致癌作用的影响。选择这些维生素和矿物质是因为近年来它们在多种致癌模型中得到了广泛研究。维生素A及其前体（类胡萝卜素）的摄入量与多个部位的癌症，尤其是肺癌呈负相关。关于维生素A参与致癌作用的动物研究一般有三种类型：评估维生素A缺乏的影响、过量维生素A的影响或补充维生素A合成类似物的影响。维生素A缺乏对唾液腺癌的发生没有影响，增强了膀胱癌、肺癌和肝癌的发生，并抑制了结肠癌的发生。各种形式的维生素A过量增强或抑制皮肤肿瘤发生，抑制大鼠（但不抑制小鼠）的乳腺癌发生，以及前胃、肝脏和膀胱癌的发生（在一种模型中，但在另一种模型中没有），或者增强或不影响肺癌的发生。维生素A类似物增强或抑制皮肤肿瘤发生，抑制唾液腺、乳腺和膀胱癌的发生，增强气管和肝癌的发生，并且根据所采用的模型，增强或抑制胰腺癌的发生。尽管类视黄醇已被证明在许多部位抑制致癌作用，但也有大量负面研究报道，并且一些报告表明会增强致癌作用。维生素C参与癌症预防最有说服力的证据是抗坏血酸能够预防亚硝胺和其他N -亚硝基化合物的形成。此外，补充维生素C被证明可抑制皮肤、鼻、气管、肺和肾癌的发生，对皮肤、乳腺和结肠癌的发生要么没有影响，要么增强，并且当以抗坏血酸钠形式给予时增强膀胱癌的发生，但以抗坏血酸形式给予时则不然。与维生素C一样，维生素E可以抑制亚硝化作用。维生素E被证明可抑制皮肤、颊囊和前胃癌的发生，增强或抑制结肠癌的发生，并且根据维生素E的给药方法或饮食中硒或膳食脂肪的水平，对乳腺癌的发生没有影响或抑制其发生。最近对硒对致癌作用的影响进行了综述，目前的讨论仅通过指出在肝脏、胰腺和皮肤中观察到膳食补充硒会增强致癌作用来更新这一领域。（摘要截取自400字）
