{"title":"Ochratoxin A in food and feed: occurrence, legislation and mode of action.","authors":"D Höhler","doi":"10.1007/pl00007368","DOIUrl":null,"url":null,"abstract":"<p><p>Ochratoxins, of which ochratoxin A (OA) is the most prevalent, are secondary fungal metabolites of some toxigenic species of Aspergillus and Penicillium. OA has been shown to be nephrotoxic, hepatotoxic, teratogenic, carcinogenic and immunosuppressive. The natural occurrence of OA in food and feed stuffs is widespread, especially in temperate areas such as Canada, Denmark, Germany, Sweden and the United Kingdom, and detectable amounts were even found in randomly collected human milk samples in Germany, Sweden and Italy. Of greatest concern in humans is its implicated role in an irreversible and fatal kidney disease referred to as Balkan Endemic Nephropathy. The mean dietary intake for humans in the European Union was found to be in the range of 1 to 2 ng/kg bw/day. Compared with the Provisional Tolerable Daily Intake (PTDI) proposed by the WHO of 16 ng OA/kg bw/day for humans, the average OA intake in Europe seems to be rather low. The main contributor to the OA intake in humans are cereals and cereal products, other possible contributors are coffee, beer, pork, products containing pig blood/plasma, pulses and spices. Only very few countries have regulations for OA in food and feed products. Based on the current literature, the mechanisms involved in the toxicity of OA indicate three major effects: (1) inhibition of mitochondrial respiration correlated with a depletion of ATP; (2) inhibition of tRNA-synthetase accompanied by a reduced protein synthesis; and (3) enhanced lipid peroxidation. Generation of free radicals and lipid peroxidation as an important mode of action of OA in vitro and in vivo is discussed in detail, as well as counteracting effects of dietary antioxidants.</p>","PeriodicalId":23811,"journal":{"name":"Zeitschrift fur Ernahrungswissenschaft","volume":"37 1","pages":"2-12"},"PeriodicalIF":0.0000,"publicationDate":"1998-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/pl00007368","citationCount":"114","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Zeitschrift fur Ernahrungswissenschaft","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/pl00007368","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 114
Abstract
Ochratoxins, of which ochratoxin A (OA) is the most prevalent, are secondary fungal metabolites of some toxigenic species of Aspergillus and Penicillium. OA has been shown to be nephrotoxic, hepatotoxic, teratogenic, carcinogenic and immunosuppressive. The natural occurrence of OA in food and feed stuffs is widespread, especially in temperate areas such as Canada, Denmark, Germany, Sweden and the United Kingdom, and detectable amounts were even found in randomly collected human milk samples in Germany, Sweden and Italy. Of greatest concern in humans is its implicated role in an irreversible and fatal kidney disease referred to as Balkan Endemic Nephropathy. The mean dietary intake for humans in the European Union was found to be in the range of 1 to 2 ng/kg bw/day. Compared with the Provisional Tolerable Daily Intake (PTDI) proposed by the WHO of 16 ng OA/kg bw/day for humans, the average OA intake in Europe seems to be rather low. The main contributor to the OA intake in humans are cereals and cereal products, other possible contributors are coffee, beer, pork, products containing pig blood/plasma, pulses and spices. Only very few countries have regulations for OA in food and feed products. Based on the current literature, the mechanisms involved in the toxicity of OA indicate three major effects: (1) inhibition of mitochondrial respiration correlated with a depletion of ATP; (2) inhibition of tRNA-synthetase accompanied by a reduced protein synthesis; and (3) enhanced lipid peroxidation. Generation of free radicals and lipid peroxidation as an important mode of action of OA in vitro and in vivo is discussed in detail, as well as counteracting effects of dietary antioxidants.
赭曲霉毒素(ochratoxin A, OA)是曲霉和青霉的次生代谢产物,其中以赭曲霉毒素A (ochratoxin A, OA)最为普遍。OA已被证明具有肾毒性、肝毒性、致畸性、致癌性和免疫抑制性。天然存在于食品和饲料中的OA很普遍,特别是在加拿大、丹麦、德国、瑞典和英国等温带地区,甚至在德国、瑞典和意大利随机收集的人乳样本中也发现了可检测到的OA。在人类中最令人关注的是它在一种被称为巴尔干地方性肾病的不可逆转和致命的肾脏疾病中所涉及的作用。在欧盟,人类的平均膳食摄入量在1至2纳克/千克体重/天。与世界卫生组织提出的人类临时每日可耐受摄入量(PTDI)为每公斤体重/天16纳克OA相比,欧洲的OA平均摄入量似乎相当低。人类摄入OA的主要来源是谷物和谷物制品,其他可能的来源是咖啡、啤酒、猪肉、含有猪血/血浆的产品、豆类和香料。只有极少数国家对食品和饲料产品中的OA有规定。根据目前的文献,OA毒性的机制主要有三个方面:(1)线粒体呼吸的抑制与ATP的消耗相关;(2) trna合成酶的抑制伴随着蛋白合成的减少;(3)增强脂质过氧化。本文详细讨论了自由基生成和脂质过氧化作为OA在体外和体内的重要作用方式,以及膳食抗氧化剂的对抗作用。