Anguidin

Aflatoxin B1 is the most potent hepatocarcinogen among the naturally occurring compounds. It's carcinogenic effect was confirmed by longterm-studies in several animal species. There exists detailed knowledge on the molecular mechanism of the carcinogenic effect caused by aflatoxin B1. At present there does not exist a reliable evidence that human primary hepatocellular carcinoma is caused by aflatoxins. Sterigmatocystin is a hepatocarcinogen too. The genotoxicity of sterigmatocystin likewise as of aflatoxin B1 was detected by short-term-tests with microbial systems and mammalian cells in vitro. It is disputable whether ochratoxin A, citrinin and T-2 toxin are carcinogenic or not. Diacetoxyscirpenol, zearalenone and patulin are estimated as not carcinogenic after longterm-studies with oral toxin administration. Patulin and penicillic acid are genotoxic in microbial systems respectively in mammalian cells in vitro. Luteoskyrin is carcinogenic, but there was not detected any genotoxicity.

Trichothecenes are a group of mycotoxins mainly produced by the fungi of Fusarium genus. Consumers are particularly concerned over the toxicity and food safety of trichothecenes and their metabolites from food-producing animals. The metabolism of T-2 toxin, deoxynivalenol (DON), nivalenol (NIV), fusarenon-X (FX), diacetoxyscirpenol (DAS), 3-acetyldeoxy-nivalenol (3-aDON), and 15-acetyldeoxynivalenol (15-aDON) in rodents, swine, ruminants, poultry, and humans are reviewed in this article. Metabolic pathways of these mycotoxins are very different. The major metabolic pathways of T-2 toxin in animals are hydrolysis, hydroxylation, de-epoxidation, and conjugation. After being transformed to HT-2 toxin, it undergoes further hydroxylation at C-3' to yield 3'-hydroxy-HT-2 toxin, which is considered as an activation pathway, whereas transformation from T-2 to T-2 tetraol is an inactivation pathway in animals. The typical metabolites of T-2 toxin in animals are HT-2 toxin, T-2 triol, T-2 tetraol, neosolaniol (NEO), 3'-hydroxy-HT-2, and 3'-hydroxy-T-2, whereas HT-2 toxin is the main metabolite in humans. De-epoxidation is an important pathway for detoxification in animals. De-epoxy products, DOM-1, and de-epoxy-NIV are the main metabolites of DON and NIV in most animals, respectively. However, the two metabolites are not found in humans. Deacetyl can occur rapidly on the acetyl derivatives, 3-aDON, 15-aDON, and FX. DAS is metabolized in animals to 15-monoacetoxyscirpenol (15-MAS) via C-4 deacetylation and then transformed to scirpentriol (SCP) via C-15 deacetylation. Finally, the epoxy is lost, yielding de-epoxy-SCP. De-epoxy-15-MAS is also the main metabolite of DAS. 15-MAS is the main metabolite in human skin. The review on the metabolism of trichothecenes will help one to well understand the fate of these toxins' future in animals and humans, as well as provide basic information for the risk assessment of them for food safety.

Multiple mycotoxins were tested in milled rice samples (n= 200) from traders at different milling points within the Mwea Irrigation Scheme in Kenya. Traders provided the names of the cultivar, village where paddy was cultivated, sampling locality, miller, and month of paddy harvest between 2018 and 2019. Aflatoxin, citrinin, fumonisin, ochratoxin A, diacetoxyscirpenol, T2, HT2, and sterigmatocystin were analyzed using ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS). Deoxynivalenol was tested using enzyme-linked immunosorbent assay (ELISA). Mycotoxins occurred in ranges and frequencies in the following order: sterigmatocystin (0-7 ppb; 74.5%), aflatoxin (0-993 ppb; 55.5%), citrinin (0-9 ppb; 55.5%), ochratoxin A (0-110 ppb; 30%), fumonisin (0-76 ppb; 26%), diacetoxyscirpenol (0-24 ppb; 20.5%), and combined HT2 + T2 (0-62 ppb; 14.5%), and deoxynivalenol was detected in only one sample at 510 ppb. Overall, low amounts of toxins were observed in rice with a low frequency of samples above the regulatory limits for aflatoxin, 13.5%; ochratoxin A, 6%; and HT2 + T2, 0.5%. The maximum co-contamination was for 3.5% samples with six toxins in different combinations. The rice cultivar, paddy environment, time of harvest, and millers influenced the occurrence of different mycotoxins. There is a need to establish integrated approaches for the mitigation of mycotoxin accumulation in the Kenyan rice.