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Yessotoxin (YTX) is a polyether. There are more than 90 known derivatives of yessotoxin. YTX was excluded from diarrhea toxins group as it, unlike okadaic acid, doesn't cause diarrhea. YTX chemical structure is similar to that of brevetoxins and ciguatoxins that influence functioning of calcium-sodium pump and trans-membrane ion channels. So, YTX can exert influence on functioning of all the organs and systems in a body. YTX is known to promote apoptosis in the cerebral tissues. Average lethal dose LD50 for YTX and its analogues varied from 100 µg/kg to 500-750 µg/kg; the figures were obtained in various experiments performed on mice. Safe YTX level for acute impact (acute reference dose) amounts to 25 μM/kg of body weight. Nowadays toxicity parameters for YTX and some of its analogues are determined; its basic action mechanisms and a role it plays in promoting apoptosis are well-known. In spite of more and more data on biological effects produced by YTX on a warm-blooded organism, experts are still unable to describe its action mechanisms precisely. Our research goal was to examine YTX toxicity in experiments in vivo in doses that were lower than the detected acute reference dose. The experiment was performed on 72 male Wistar rats with initial body weight being equal to 100±10 г. Animals were given dry balanced feedstuff produced by "Laboratortakorm" LLC (Russia) and had free access to it. We used YTX preparation produced by "National Research Council Canada" (Canada) in our experiment; the preparation was a methanol solution (YTX content was equal to 4.3 µmol). We determined mass of internal organs, biochemical and hematological blood parameters, apoptosis of brain cells, malonic dialdehyde level in the brain and reduced glutathione in the liver. We showed that YTX doses (2μM/kg, 8μM/kg and 12μM/kg) lower than ARfD=2μM/kg can exert toxic impacts on a warm-blooded organism. The obtain data prove it is necessary to additionally assess risks of an increase in maximum permissible YTX contents in shellfish from 1 mg/kg to 3.75 mg/kg.

The performed research is truly vital, as As (arsenic) concentration in food products is now of great interest. The US ATSDR and EPA enlist As among the most toxic substances which are dangerous for human health. We suggest a procedure for separate quantitative mass fraction determination for organic (oAs) and non-organic (iAs) arsenic compounds in sea products with solid phase extraction (SPE) application combined with atomic adsorption spectrometry. Samples were prepared according to the following procedure: liquid extraction phase with simultaneous As (III) oxidation into As (IV) with hydrogen peroxide and As (V) extraction into a 0.055 M liquid phase with hydrochloric acid. Arsenic organic and non-organic compounds were separated via solid phase extraction with Strata SAX cartridges (Sorbent Lot Number: S208-0058). To quantitatively assess the obtained samples, we applied atomic-adsorption techniques for As determination with "KVANT-2A-GRG" spectrometer according to the State Standard 51766-2001. We revealed that common As concentration didn't conform to fixed standards in 8 out of 17 analyzed samples (2 shrimps, 1 crab, 1 fish, and 4 seaweeds). However, iAs concen-tration was significantly lower than oAs concentration in all the samples. 6 out of 17 analyzed samples didn't contain any iAs within detection limits (0.1 mg/kg), and apparently all the As concentration occurred due to its organic compounds. The suggested procedure for separate oAs and iAs detection is relatively simple in terms of devices applied in it, and quite cheap, as SPE cartridges needed to perform it can be re-used after re-conditioning. This procedure, after a proper metrological validation, can be implemented in most laboratories which are certified to examine chemical safety of food products.

Okadaic acid (OA) is relating to the number of seafood toxins causing diarrhea. At the present time, there was determined the toxicity index of OA; the main target molecules of its action, its role as a promoter of tumor processes and apoptosis have been investigated. However, in the available literature, data on the toxicokinetics of OA and molecular biomarkers of its action for warm-blooded animals are practically absent. The purpose of this work was to determine biomarkers of toxicity of OA in experiments in vivo and ex vivo. The experiment was performed on 74 male Wistar rats with an initial body weight of 100 ± 10 g. In the work, there was used a solution of OA in methanol, produced by “FermentecLtd.” (Israel). Prior to the studies, methanol was removed from the preparation. To obtain working dilutions of the toxin, aliquots of the alcoholic OA solution with a concentration of 10 ppm were diluted with a sterile solution of 0.15M NaCl to obtain solutions with a concentration of OA of 50, 100 and 150 ppb. These solutions were administered to the rats in doses of 1 ml/kg of body weight intraperitoneally. The animals of the control groups were injected with NaCl solution. Excretion of animals from the experiment was carried out 6, 24 and 168 hours after the administration of OA preparations by decapitation under ether anesthesia. The mass of internal organs, biochemical and hematological blood indices, the activity of glutathione peroxidase, non-protein thiols in the liver, cytokine levels of IFN-ɤ, IL-10, IL-17A in blood plasma and liver cell lysates, liver cell apoptosis, malonic dialdehyde level in the liver were analyzed. Studies have shown minimal manifestations of toxic effects of OA in case of intraperitoneal administration (shifts in the ratio of neutrophils and lymphocytes, increased activity of AST, changes in the activity of glutathione peroxidase) to be observed even at a dose of 50 μg/kg of body weight. Taking into account the safety factor of 3, the ARfD level of OA should be revised and accepted to be equal to 0.27 μg/kg of body weight. The data obtained indicate the need for additional risk assessments of this toxin for the health of consumers and, possibly, a revision of the established values of the safe content of this toxin in mollusks. For the first time, there was shown the possibility of using the following marker of toxic action of OA: non-protein thiols, the activity of glutathione peroxidase, and the content of malonic dialdehyde in the liver.