The white beetroot cv. Śnieżna Kula is the first betanin-free beetroot registered in the European Union. The aim of this study was to compare the phenolic acids profile and antioxidant capacity of leaves of white (SK) and red (CC) beetroots and red (LC) and white (BL) Swiss chard growing in Poland. LC leaves were the richest source of total phenolics (16.55 mg GAE/g FW) and phenolic acids (1.81 mg/g FW), while the highest content of flavonoids was determined in CC leaves (1.6 mg QE/g FW). The highest antiradical activity was observed for LC, whereas CC extract exhibited the highest chelating power. BL and CC leaf extracts demonstrated high LOX inhibitory potential (EC₅₀ = 53.23 and 56.97 mg FW/mL, respectively). An uncompetitive type of LOX inhibition was obtained for all extracts. SK extracts demonstrated the highest XO inhibitory activity (EC₅₀ = 81.04 mg FW/mL). A noncompetitive type of XO inhibition was obtained in both extracts from red leaves (CC and LC), whereas an uncompetitive mode of inhibition was observed in the case of white leaf (SK and LC) extracts. Thus, it can be assumed that the presence of betanin influences the XO inhibition mechanism.

Vitamin D3 deficiency has been recognized as a pandemic with serious health consequences including chronic respiratory diseases. Unfortunately, improvement in this situation by using vitamin D supplementation has failed. The direct delivery of 1,25(OH)₂-vitamin D3 and its precursor into the respiratory tract, by nebulization, seemed to be a better option, as verified in the presented study. To induce vitamin D deficiency, mice received a diet with 0.05 IU/g cholecalciferol, while control animals were given feed with 0.5 IU/g cholecalciferol. Vitamin-D-deficient mice were exposed to different doses of calcidiol or calcitriol via nebulization for at least 7 days. At the end of the experiment, whole-body plethysmography was conducted. Pulmonary and serum levels of calcitriol were examined using ELISA. The calcitriol concentrations in mice on standard vs. deficient diet were 30.31/18.20 pg/mg (lungs) and 132.24/98.61 pg/mL (serum), respectively. Restoration of the physiological level of calcitriol in vitamin-D-deficient mice required 1-week exposure to 100 pg/g of calcidiol or 5 pg/g of calcitriol. The inhalations did not cause any side changes in murine respiratory function. The presented study revealed the usefulness and safety of chronic inhalation with a bioactive form of vitamin D3 or its precursor for the restoration of physiological calcitriol levels in animals with vitamin D deficiencies.

Despite numerous scientific reports on the negative impact of vitamin D3 deficiency on many respiratory diseases, little is known about the influence of this phenomenon on the development and progression of hypersensitivity pneumonitis (HP). The presented study is an attempt to shed light on this occurrence. The research was performed on mouse strain C57BL/6J exposed to the antigen of Pantoea agglomerans (etiological factor of HP). To induce vitamin D3 deficiency, mice received a diet with a 10 times lower amount of cholecalciferol than the main control group. VD3-deficient mice inhaled 25(OH)-VD3 or 1,25(OH)2-VD3 used separately or with SE-PA. At the beginning of the experiment and after 14 and 28 days of inhalation, respiratory function was examined using whole-body plethysmography. Moreover, at indicated time points, mice were sacrificed and samples collected for histological examination, flow cytometry, and ELISA. The performed study revealed that inhalations with 25(OH)-VD3 and 1,25(OH)2-VD3 effectively eliminated most of the negative changes in the respiratory system caused by vitamin D3 deficiency by restoring the physiological concentration of 1,25(OH)₂-VD3 in the body. VD3-deficient mice which inhaled P. agglomerans antigen and vitamin D3 metabolites also demonstrated the ability of the tested compounds to eliminate, or at least weaken, the negative effects of the HP causative factor and desired effect, including improvement of respiratory functions and attenuation of inflammation and signs of fibrosis. The obtained results suggested that the beneficial influence of inhaled vitamin D3 metabolites on HP development was associated with the restoration of the physiological concentration of 1,25(OH)2-VD3 in the pulmonary compartments in VD3-deficient mice.

Although vitamin D3 (VD3) deficiency has been recognized as a harmful agent in several respiratory diseases, the present study is the first one to investigate its influence on the development of hypersensitivity pneumonitis (HP). This research was conducted in a murine model of HP, wherein pulmonary fibrosis was induced by antigen of Pantoea agglomerans. VD3 deficiency was provoked by diet with 10-times less cholecalciferol than feed given to VD3-sufficient mice. Before and after 14 and 28 days of nebulization, lung function was evaluated. Moreover, at indicated time points, lungs were collected and subjected to histological assessment, flow cytometry, gene expression assays, and ELISA. The performed research showed a higher sensitivity of VD3-deficient mice to fibrosis response to P. agglomerans antigen, which was strongly associated with enhanced epithelial-to-mesenchymal transition, the signs of which were over-expression of EMT-transcription factors (Snail2, Zeb1, Zeb2) and mesenchymal cell markers (Cdh2/N-cadherin, Acta2/SMA, Fn1/Fibronectin, Vim/Vimentin). Indicated negative changes in VD3-deficient mice with developed HP were supported by deepening calcitriol deficiency and worsening respiratory functions, including the frequency of breathing, minute volume, total cycle times, expiratory and inspiratory time. Moreover, typical for VD3-deficient mice with HP, there was also an increased influx of immune cells into the lungs (especially neutrophils, macrophages, dendritic cells and lymphocytes Tc), a disturbed cytokine profile with over-production of growth factors favoring fibrosis (FGF2 and TGFβ), and lowered synthesis of several cytokines (IL1β, IL6, IL12, IL4 IL10, IL13). The present study reveals that VD3 deficiency promotes the development of pulmonary fibrosis in the murine model of HP.

Wirusy onkogenne to wirusy zdolne do indukowania procesu nowotworzenia. Zaliczają się do nich: wirus zapalenia wątroby typu B (HBV), wirus zapalenia wątroby typu C (HCV), wirus Epsteina-Barr (EBV), wirus brodawczaka ludzkiego (HPV), wirus mięsaka Kaposiego (KSHV), ludzki wirus T-limfotropowy typu 1 (HTLV-1) i poliomawirus komórek Merkla (MCPV). Mechanizm działania wirusów onkogennych polega na inaktywacji białkowych produktów genów supresorowych komórki gospodarza bądź na wbudowaniu do genomu docelowej komórki własnych onkogenów. Prowadzi to do zakłóceń cyklu komórkowego, nadmiernej proliferacji, a w konsekwencji do powstania guza. W niniejszej pracy przedstawiono charakterystykę wirusów onkogennych: EBV, HPV, HBV, HCV, w oparciu o aktualne doniesienia naukowe oraz nowoczesne metody leczenia i zapobiegania infekcjom przez nie wywoływanym. Około 15–20% zachorowań na nowotwory ma podłoże infekcyjne. Wśród biologicznych czynników ryzyka karcenogenezy wyróżnia się zakażenia bakteryjne, zarażenia pasożytnicze oraz występujące najczęściej zakażenia o etiologii wirusowej. Przewlekłe zakażenie EBV, HPV, HCV bądź HBV wiąże się z występowaniem odpowiednio takich nowotworów, jak: chłoniak Burkitta, rak szyjki macicy, rak wątroby. Odkrycie znaczącej roli wirusów onkogennych w karcenogenezie stwarza nowe perspektywy w zapobieganiu i terapii niektórych chorób nowotworowych. Ze względu na powszechność występowania wirusów onkogennych i ograniczone możliwości leczenia szczególnie istotne jest zwiększanie świadomości społecznej i zachęcanie do stosowania działań prewencyjnych, a także prowadzenie dalszych badań w celu ustalenia dokładnego mechanizmu karcenogenezy indukowanej infekcjami wirusowymi.

Niektóre wirusy są zdolne do indukcji procesu nowotworzenia. Szacuje się, że wśród czynników ryzyka karcynogenezy 15–20% stanowią czynniki infekcyjne, w tym wirusy onkogenne. Celem niniejszej pracy było przedstawienie charakterystyki wybranych wirusów onkogennych, takich jak KSHV, HTLV i MCPV, oraz wykazanie ich udziału w proces nowotworzenia. Do wirusów onkogennych, zdolnych do indukcji procesu nowotworzenia, zaliczają się: EBV, HPV, HBV, HCV, KSHV, HTLV oraz MCPV. Wirusy te kodują onkoproteiny, które oddziałują na wiele szlaków sygnałowych, zakłócając funkcje białek w komórce gospodarza, co przyczynia się do rozregulowania cyklu komórkowego i zaburzenia stabilności genetycznej komórki gospodarza. Najważniejszą onkoproteiną wirusa KSHV jest LANA, która inhibuje białka p53 i pRB, wpływając na osłabienie apoptozy zakażonych komórek. W procesie transformacji nowotworowej wirusa HTLV-1 bierze udział białko Tax, które zaburza cykl i proliferację komórkową komórek gospodarza. Wirus MCPV z kolei koduje dwie ważne onkoproteiny wirusowe: LT oraz sT. Aktualny stan wiedzy na temat udziału wirusów w procesie nowotworzenia wymaga dalszego prowadzenia badań i pogłębienia wiedzy.