Bailey G S, Williams D E, Hendricks J D
Department of Food Science and Technology, Oregon State University, Corvallis 97331, USA.
Environ Health Perspect. 1996 Mar;104 Suppl 1(Suppl 1):5-21. doi: 10.1289/ehp.96104s15.
Progress over the past 30 years has revealed many strengths of the rainbow trout as an alternative model for environmental carcinogenesis research. These include low rearing costs, an early life-stage ultrasensitive bioassay, sensitivity to many classes of carcinogen, a well-described tumor pathology, responsiveness to tumor promoters and inhibitors, and a mechanistically informative nonmammalian comparative status. Low-cost husbandry, for example, has permitted statistically challenging tumor study designs with up to 10,000 trout to investigate the quantitative interrelationships among carcinogen dose, anticarcinogen dose, DNA adduct formation, and final tumor outcome. The basic elements of the trout carcinogen bioassay include multiple exposure routes, carcinogen response, husbandry requirements, and pathology. The principal known neoplasms occur in liver (mixed hepatocellular/cholangiocellular adenoma and carcinoma, hepatocellular carcinoma), kidney (nephroblastoma), swim bladder (adenopapilloma), and stomach (adenopapilloma). Trout possess a complex but incompletely characterized array of cytochromes P450, transferases, and other enzymic systems for phase I and phase II procarcinogen metabolism. In general, trout exhibit only limited capacity for DNA repair, especially for removal of bulky DNA adducts. This factor, together with a high capacity for P450 bioactivation and negligible glutathione transferase-mediated detoxication of the epoxide, accounts for the exceptional sensitivity of trout to aflatoxin B1 carcinogenesis. At the gene level, all trout tumors except nephroblastoma exhibit variable and often high incidences of oncogenic Ki-ras gene mutations. Mutations in the trout p53 tumor suppressor gene have yet to be described. There are many aspects of the trout model, especially the lack of complete organ homology, that limit its application as a surrogate for human cancer research. Within these limitations, however, it is apparent that trout and other fish models can serve as highly useful adjuncts to conventional rodent models in the study of environmental carcinogenesis and its modulation. For some problems, fish models can provide wholly unique approaches.
过去30年的进展揭示了虹鳟鱼作为环境致癌研究替代模型的诸多优势。这些优势包括养殖成本低、生命早期超灵敏生物测定法、对多种致癌物敏感、肿瘤病理学描述详尽、对肿瘤促进剂和抑制剂有反应以及具有提供机制信息的非哺乳动物比较地位。例如,低成本养殖使得能够采用具有统计学挑战性的肿瘤研究设计,使用多达10,000条虹鳟鱼来研究致癌物剂量、抗癌剂剂量、DNA加合物形成和最终肿瘤结果之间的定量相互关系。虹鳟鱼致癌物生物测定的基本要素包括多种暴露途径、致癌物反应、养殖要求和病理学。已知的主要肿瘤发生在肝脏(混合性肝细胞/胆管细胞腺瘤和癌、肝细胞癌)、肾脏(肾母细胞瘤)、鳔(腺乳头状瘤)和胃(腺乳头状瘤)。虹鳟鱼拥有一系列复杂但特征不完全明确的细胞色素P450、转移酶和其他用于I期和II期前致癌物代谢的酶系统。一般来说,虹鳟鱼的DNA修复能力有限,尤其是去除大分子DNA加合物的能力。这个因素,加上P450生物活化能力高以及谷胱甘肽转移酶介导的环氧化物解毒作用可忽略不计,导致虹鳟鱼对黄曲霉毒素B1致癌作用异常敏感。在基因水平上,除肾母细胞瘤外,所有虹鳟鱼肿瘤都表现出致癌性Ki-ras基因突变的发生率可变且往往很高。虹鳟鱼p53肿瘤抑制基因的突变尚未见报道。虹鳟鱼模型有许多方面,尤其是缺乏完全的器官同源性,这限制了它作为人类癌症研究替代模型的应用。然而,在这些限制范围内,很明显虹鳟鱼和其他鱼类模型在环境致癌及其调节研究中可作为传统啮齿动物模型非常有用的辅助模型。对于某些问题,鱼类模型可以提供完全独特的方法。