Rose F J
Environ Qual Saf Suppl. 1976(5):227-37.
It has long been known that certain estrogens and testosterone may increase, or sometime decrease, the incidence of neoplasmas in laboratory animals. They probably act by switching-on inappropriate genetic information or switching-off appropriate genetic information contained in nucleic acids. For instance, they may switch-on in adult animals information which is relevant only to a certain stage of embryogenesis or they may facilitate the expression of oncogenic viruses which would otherwise lay harmlessly dormant. The situation is rendered complex because an effect on one endocrine gland leads to effects on others so that factors which favour tumour development may result indirectly from administration of an anabolic or other hormonal agent. Two kinds of neoplasm are now known to be associated with human exposure to anabolic agents: vaginal adenocarcinoma and liver-cell tumours. Tumours of both kinds are among the spectrum of neoplasms that has been seen in laboratory animals exposed to agents of the same kind. In both animals and man there is evidence that tumours arising in response to anabolic agents are sometimes, initially at least, hormone-dependent. The evidence that 17beta-estradiol, diethylstilbestrol, chlormadinone, and testosterone are carcinogenic for laboratory animals is briefly reviewed and the reader's attention is directed towards the 1974 IARC Monograph on the evaluation of sex hormones for carcinogenic risk to man where the same evidence is reviewed more extensively. The significance for man of the results of studies on laboratory animals is discussed with special reference to the use of anabolic agents in meat production. Non-residue uses are to be preferred, as are naturally-occurring agents as opposed to compounds which do not occur in nature. More information is needed concerning the possible effects of prolonged exposure to very low doses of anabolic agents.
长期以来人们都知道，某些雌激素和睾酮可能会增加，或者有时会降低实验动物肿瘤的发生率。它们可能通过开启不适当的遗传信息或关闭核酸中包含的适当遗传信息来发挥作用。例如，它们可能在成年动物中开启仅与胚胎发育某一阶段相关的信息，或者它们可能促进致癌病毒的表达，否则这些病毒会无害地处于休眠状态。情况变得复杂，因为对一个内分泌腺的影响会导致对其他内分泌腺的影响，以至于有利于肿瘤发展的因素可能间接源于给予合成代谢剂或其他激素制剂。现已知道两种肿瘤与人接触合成代谢剂有关：阴道腺癌和肝细胞肿瘤。这两种肿瘤都在接触同类制剂的实验动物所出现的肿瘤范围内。在动物和人类中都有证据表明，因合成代谢剂而产生的肿瘤有时至少在最初是激素依赖性的。本文简要回顾了17β-雌二醇、己烯雌酚、氯地孕酮和睾酮对实验动物具有致癌性的证据，并引导读者关注1974年国际癌症研究机构关于评估性激素对人类致癌风险的专论，其中对相同证据进行了更广泛的回顾。本文特别参照在肉类生产中使用合成代谢剂的情况，讨论了实验动物研究结果对人类的意义。应优先选择无残留用途，天然存在的制剂也比自然界中不存在的化合物更受青睐。关于长期接触极低剂量合成代谢剂可能产生的影响，还需要更多信息。
