Free radicals generated in ethanol metabolism may be responsible for tumor promoting effects of ethanol.
Free radicals generated in ethanol metabolism may be responsible for tumor promoting effects of ethanol.
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乙醇代谢中产生的自由基可能是乙醇促进肿瘤作用的原因。
DOI：
10.1007/978-1-4684-5877-0_105
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发表时间：
1991
影响因子：
--
通讯作者：
Mufti,SI
中科院分区：
文献类型：
--
作者：
Mufti,SI
长期饮酒被认为是人类癌症的一个主要危险因素[例如，Hakulinen等人，1974；Breslow and Enstrom, 1974；Feldman et al., 1975；Williams and Horm, 1977；Schottenfeld, 1979;河野和池田，1979；Tuyns, 1979;Doll and Peto, 1981]。与酒精相关癌症相关的主要部位是口腔、食道和肝脏[Hakulinen et al., 1974；Breslow and Enstrom, 1974；Feldman et al., 1975；河野和池田，1979；Rothman et al., 1980；Tuyns, 1982;Vassallo et al., 1985]，美国75%的食管癌和36%的肝癌可归因于过度饮酒[Rothman et al., 1980]。然而，尽管有强有力的流行病学证据，但这种关联的实验证据并不明确，而且经常得到相互矛盾的结果[Schmahl et al., 1965；Gibel, 1967;Schmahl, 1976;Griciute et al., 1982；Gabrial et al., 1982；Habs和Schmahl, 1981；Teschke et al., 1983；McCoy et al., 1986]。为了阐明乙醇的作用，我们最近开展了一些研究，在癌变开始时或癌变完成后，将乙醇作为肿瘤启动子使用[Mufti等，1989]。我们的研究结果显示，乙醇仅在食道特异性致癌物n -亚硝基甲基苄胺（NMBzA）治疗完成后才会增加食道肿瘤的发生率。然而，在n -亚硝基二乙胺（NDEA）诱导的致癌研究中，我们没有发现肝脏肿瘤或γ谷氨酰转肽酶改变的肝岛的增加可归因于乙醇的促肿瘤作用[Mufti和Sipes， 1990]。本文是我们对酒精相关致癌机制的初步研究报告，可以用来解释乙醇与NMBzA-和ndea诱导的致癌作用的矛盾作用。
Chronic alcohol consumption is considered a major risk factor for human cancers [for example, Hakulinen et al., 1974; Breslow and Enstrom, 1974; Feldman et al., 1975; Williams and Horm, 1977; Schottenfeld, 1979; Kono and Ikeda, 1979; Tuyns, 1979; Doll and Peto, 1981]. The main sites associated with alcohol-related cancers are the oral cavity, esophagus and liver [Hakulinen et al., 1974; Breslow and Enstrom, 1974; Feldman et al., 1975; Kono and Ikeda, 1979; Rothman et al., 1980; Tuyns, 1982; Vassallo et al., 1985] and 75% of esophageal cancers and 36% of hepatic cancers in the U.S.A. are attributable to excessive alcohol consumption [Rothman et al., 1980]. Despite the strong epidemiologic evidence, however, experimental evidence for the association is not clear and often contradictory results have been obtained [Schmahl et al., 1965; Gibel, 1967; Schmahl, 1976; Griciute et al., 1982; Gabrial et al., 1982; Habs and Schmahl, 1981; Teschke et al., 1983; McCoy et al., 1986]. In order to clarify the role of ethanol, recently we carried out studies where ethanol was administered either during the initiation of carcinogenesis or later as a tumor promoter after initiation with the carcinogen was completed [Mufti et al., 1989]. Our results showed that ethanol increased esophageal tumor incidence only when administered after treatment with esophagus specific carcinogen, N-nitrosomethylbenzylamine (NMBzA) was completed. However, in studies of carcinogenesis induced by N-nitrosodiethylamine (NDEA), reported in another article in these proceedings, we did not find an increase either in liver tumors or gamma glutamyltranspeptidase-altered hepatic islands that could be attributed to the tumor promoting effects of ethanol [Mufti and Sipes, 1990]. This paper is a preliminary report of our investigations into the mechanisms of alcohol-related carcinogenesis that could be used to explain the contradictory effects of ethanol obtained with NMBzA- and NDEA-induced carcinogenesis.