The authors performed screening of a wide range of mycotoxins by ultra-high-performance liquid chromatography combined with tandem mass spectrometry (UHPLC-MS/MS) in various tea products distributed on the RF market. Samples were selected in retail outlets and obtained from wholesalers. Seventy-seven tea samples were examined: 54 out of them were Camellia sinensis tea, not packed (semi-finished product) and packed; 23 were mono-and multi-component herbal tea. The analytes were 29 mycotoxins including regulated in food products (aflatoxins, ochratoxin A, deoxynivalenol, fumonisins, T-2 toxin and zearalenone), their derivatives and structural analogues (A and B trichothecenes, structural analogues of zearalenone); emergent mycotoxins (sterigmatocystin, mycophenolic acid, moniliformin, enniatins, beauvericin and Alternaria toxins). C. sinensis tea samples, both green and black, were the least contaminated. In contrast, multi-component herbal tea samples tended to be simultaneously contaminated with several mycotoxins (over five) both regulated in food products and emergent ones. Beauvericin, mycophenolic acid and enniatin B were the most frequently detected. Toxigenic properties of mixed tea microflora were examined in vitro. Model experiments were carried out on a substrate consisting of C. sinensis green tea leaves in the absence of any growth factors. Mixed mycoflora from tea, which contained potentially toxigenic species of mold species proved to be capable to simultaneously produce substantial quantities of several mycotoxins including emergent ones. Mycotoxins accumulation amounted to 290 and 5,600 µg/kg of fumonisins B1 and B2 accordingly; 130 µg/kg of zearalenone; 14 µg/kg of sterigmatocystin; 160 µg/kg of alternariol methyl ester. The present survey indicates there is a potential health risk associated with mycotoxins in teas, especially herbal ones. The systematic study of contamination of tea products distributed in the RF with mycotoxins and their producers has been performed for the first time. Long-term monitoring over variety of mycotoxins in this kind of food products is essential for assessing its safety.

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Nanoparticles of nickel (Ni) and its compounds attract a lot of attention bearing in mind their promising innovative properties allowing their use as catalysts, components in electrical appliances, electronic devices and photonic appliances, and materials used in producing medications, diagnostic preparations, and pesticides. Production volumes of these materials in their nano-form are likely to grow rapidly in the nearest future and it involves greater loads created by these nanomaterials on a human body. And we should remember that Ni and its compounds are highly toxic for humans even in their traditional disperse forms. Their toxicity induces oxidative stress, cellular membranes and mitochondria dysfunction, expression of nuclear transcription factors that are responsible for apoptosis, caspases, as well as proto-oncogenes. Leading role in toxicity of Ni-containing nanomaterials obviously belongs to ions of heavy Ni++ being emitted from them since this heavy metal has pro-oxidant properties and influences enzyme activity and gene expression. Cytotoxic effects produced by Ni-containing nanomaterials were revealed in Model experiments in vitro performed with suing cellular cultures that were morphologically and functionally similar to epithelial cells of respiratory and gastrointestinal tract, liver, kidneys, and nervous system; these materials were able to stimulate oxidant stress, influence expression of apoptosis proteins and nuclear transcription factors, induce apoptosis and necrosis. There are data indicating that Ni-containing nanomaterials can produce malignant transforming effects in vitro. All the above mentioned proves that nickel compounds in their nanoform are a new hazardous factor that requires assessing related risks for workers, consumer, and population in general. Our review focuses on analyzing literature sources on cytotoxicity of Ni-containing nanomaterials and their effects produced on molecular-genetic and cellular levels taken over a period starting from 2011.