Pathology Department, County Hospital Timisoara, 300736 Timisoara, Romania.
Centre for Environmental Policy, Imperial College London, London SW7 2AZ, UK.
Toxins (Basel). 2021 Mar 12;13(3):205. doi: 10.3390/toxins13030205.
Mammalian animal toxicity of ochratoxin A (OTA) has focused largely in the past half-century on pigs because of initial recognition of it as a principal cause of intermittent growth suppression and renal disease caused by mouldy feed. Subsequent classical toxicology has used laboratory rodents because renal pathology in pigs raised questions concerning possible involvement in the human idiopathic bilateral renal atrophy of Balkan endemic nephropathy for which OTA was a focus of attention for human nephropathy through 1980s and into 2000s. Emphasis on human nephropathy has more recently concerned the plant metabolite aristolochic acid. Recognition that agricultural management can often minimise food and feed-stuff spoilage by OTA-producing Aspergilli and Penicillia has moderated some of the risks for animals. Legislation for human food safety combined with sophisticated analysis generally provides safety in the developed world. Chronic experimental exposure of male rats, in the absence of clinical dis-ease, specifically causes renal cancer. The possibility of this as a unique model for the human has generated considerable experimental evidence which may be more directly relevant for carcinogenesis in the complex kidney than that obtained from biochemical toxicities in vitro. Nevertheless, there does not appear to be any case of human renal or urinary tract cancer for which there is verified etiological proof for causation by OTA, contrary to much claim in the literature. To contribute to such debate, histopathology review of OTA/rat renal cancers, augmented where appropriate by immune profiles, has been completed for all remaining tumours in our research archive. Overall consistency of positivity for vimentin, is matched with occasional positives either for CD10 or the cytokeratin MNF 116. The current situation is discussed. Suggestion that OTA could cause human testicular cancer has also been challenged as unsupported by any experimental findings in rats, where the Leydig cell tumour immune profile does not match that of human germ cell neoplasms.
OTA(赭曲霉毒素 A)对哺乳动物的毒性在过去半个世纪以来主要集中在猪身上,因为最初人们认识到 OTA 是导致霉变饲料引起间歇性生长抑制和肾脏疾病的主要原因。随后的经典毒理学研究使用了实验室啮齿动物,因为猪的肾脏病理引起了人们的关注,即 OTA 是否可能参与到巴尔干地方性肾病的人类特发性双侧肾萎缩中,在 20 世纪 80 年代和 90 年代,OTA 一直是人类肾病关注的焦点。最近对人类肾病的关注更多地集中在植物代谢产物马兜铃酸上。认识到农业管理通常可以减少产 OTA 的曲霉菌和青霉菌对食物和饲料的破坏,从而降低了动物的一些风险。人类食品安全立法加上复杂的分析,在发达国家通常提供了安全性。慢性实验性暴露于雄性大鼠中,在没有临床疾病的情况下,特异性地导致肾脏癌症。这种情况作为人类特有的模型的可能性产生了大量的实验证据,这些证据可能比在体外生化毒性研究中获得的证据更直接地与肾脏的癌变相关。然而,目前似乎没有任何人类肾脏或泌尿道癌症的病例可以通过 OTA 引起的病因学证明,这与文献中的许多说法相反。为了促进这一辩论,我们对研究档案中所有剩余的肿瘤进行了 OTA/大鼠肾脏癌症的组织病理学回顾,并在适当的情况下增加了免疫谱分析。波形蛋白的阳性一致性很高,偶尔也会出现 CD10 或细胞角蛋白 MNF116 的阳性。目前的情况进行了讨论。关于 OTA 可能导致人类睾丸癌的说法也受到了挑战,因为在大鼠中没有任何实验发现支持这一说法,而睾丸间质细胞瘤的免疫谱与人类生殖细胞肿瘤的免疫谱不匹配。