An experimental study of antioxidant parameters in rats after exposure to carbendazim was carried out to study the effect of their pharmacological correction by an intragastric administration of Saccharina latissima extract at a dose of 250 mg/kg for 14 days. The extract under study was found to reduce the activity of lipid peroxidation and promote the neutralization of hydrogen peroxide.

Актуальность. Ингибирование рецептора фактора роста фибробластов 2 типа (ФРФР2) представляется целесообразным у больных с опухолями, экспрессирующими или амплифицирующими ФРФР2. Токсичность аллостерических ингибиторов ФРФР2 ранее не изучалась. Цель исследования. Оценка токсичности противоопухолевого препарата алофаниб (RPT835), аллостерического ингибитора рецептора фактора роста фибробластов 2 типа (ФРФР2), в стандартных экспериментальных моделях in vivo на грызунах и негрызунах.

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The article presents experimental data on the state of the antioxidant system in red blood cells of white outbred rats 1 and 3 months after acute mercury nitrate poisoning with a semilethal dose. It has been established that this form of intoxication is accompanied by pronounced changes in the state of the antioxidant defense system in erythrocytes of poisoned animals (a decrease in the concentration of reduced glutathione, a decrease in the activity of superoxide dismutase and glutathione peroxidase, and an increase in the concentration of lipid peroxidation products).It has been shown that the mercury content in the blood of experimental animals remains elevated during the entire study period.The results obtained indicate the importance of impaired functioning of the antioxidant system in the implementation of long-term consequences of acute mercury poisoning. The reasons for the occurrence of these biochemical shifts and their role in the development of the long-term cytotoxic effects of mercury nitrate are discussed.

e15659 Background: The incidence of cancer among the people of reproductive age is constantly increasing. Although FGF2/FGFR2 expression in the male reproductive tract has been reported, there is no evidence of the impact of FGFRs inhibitors on sperm function. Therefore, the objective of this large study was to determine the effects of alofanib, selective FGFR2 allosteric extracellular inhibitor on the regulation of sperm physiology using the rat and rabbit models. Methods: Two-hundred forty Sprague-Dawley rats and 30 Chinchilla white rabbits received alofanib (0–40.5 and 0–21.6 mg/kg/day, respectively) intravenously on a consecutive daily dosing schedule for six months. Eighty rats and 8 rabbits were in the control group. The subchronic study evaluated high doses (300 mg/kg/day) of alofanib for 2 months in 15 male rats. Necropsy was conducted following treatment/recovery periods, and histologic examinations were performed. Results: Animals were active. After injections of a dose equivalent to a human therapeutic dose during 6 months, most of the seminiferous tubules were empty, the elements of spermatogenesis were not classified, and altered primary spermatogonia and spermatocytes were distinguished in male rats. After injections of a five-fold dose, all seminiferous tubules were empty and expelled by a cylindrical epithelium. Very similar changes in sperm physiology were founded in rabbits. Most of the seminiferous tubules were blank, and some tubules contained eosinophilic amorphous masses. High doses of alofanib resulted in pronounced atrophy of the spermatogenic tubule epithelium. Multinucleated giant cells were observed in the lumen of a part of the tubules. There were no changes in untreated animals. Conclusions: FGFR2 inhibition led to the suppression of spermatogenesis. Male cancer patients should be informed of this potential adverse event before treatment with FGFR2 inhibitors.