Abstract
Since ochratoxin A (OTA) was discovered, it has been ubiquitous as a natural contaminant of moldy food and feed. The multiple toxic effects of OTA are a real threat for human beings and animal health. For example, OTA can cause porcine nephropathy but can also damage poultries. Humans exposed to OTA can develop (notably by inhalation in the development of acute renal failure within 24 h) a range of chronic disorders such as upper urothelial carcinoma. OTA plays the main role in the pathogenesis of some renal diseases including Balkan endemic nephropathy, kidney tumors occurring in certain endemic regions of the Balkan Peninsula, and chronic interstitial nephropathy occurring in Northern African countries and likely in other parts of the world. OTA leads to DNA adduct formation, which is known for its genotoxicity and carcinogenicity. The present article discusses how renal carcinogenicity and nephrotoxicity cause both oxidative stress and direct genotoxicity. Careful analyses of the data show that OTA carcinogenic effects are due to combined direct and indirect mechanisms (e.g., genotoxicity, oxidative stress, epigenetic factors). Altogether this provides strong evidence that OTA carcinogenicity can also occur in humans.
Highlights
Ochratoxin A (OTA) is one of the most important and deleterious mycotoxins [1,2].ochratoxin A (OTA) was isolated and chemically characterized in 1965 [3,4]
Findings of higher OTA levels in the serum of patients suffering from Balkan endemic nephropathy (BEN), which is a subtype of tubulointerstitial nephritis, led to hypotheses about the association between the nephrotoxicity of OTA and the BEN and the incidence of renal system tumors in the population of these Balkan regions
Nephropathy is primarily related to the mobilization of intracellular calcium
Summary
Ochratoxin A (OTA) is one of the most important and deleterious mycotoxins [1,2].OTA was isolated and chemically characterized in 1965 [3,4]. Further research has shown that OTA is nephrotoxic, hepatotoxic, embryotoxic, teratogenic, neurotoxic, immunotoxic, genotoxic, and carcinogenic in many species with species and sex-related differences [5,6,7,8,9,10]. The International Agency for Research on Cancer classified OTA as a possible human carcinogen (group 2B) in 1993 based on a great amount of evidence of its carcinogenity discovered in several animal studies [11]. OTA could be a threat of cancer for humans. It will be shown further in this article that OTA acts as a nephrotoxin and an urothelial carcinogen as a result of both the oxidative stress and direct genotoxic mechanisms.
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