Sergey Shaposhnikov

This study aimed to evaluate the impact of a more cost-efficient strigolactone mimic SL-6 on Chlorella sorokiniana NIVA-CHL 176 growth in comparison with the strigolactone analog GR24 and the plant biostimulant functions of microalgal extracts. Three molar SL-6 concentrations were tested: 10⁻⁷ M, 10⁻⁸ M, and 10⁻⁹ M, respectively. Five parameters of microalgal growth were assessed: optical density, turbidity, biomass production, chlorophyll fluorescence, and pigment concentration. Results after 15 days of culturing revealed that the SL-6 treatments significantly enhanced biomass production (13.53% at 10⁻⁹ M), pigment synthesis, and photosystem II activity (14.38% at 10⁻⁹ M). The highest increases in pigments induced by SL-6 were 15.7% for chlorophyll a (at 10⁻⁸ M SL-6), 12.87% for chlorophyll b (at 10⁻⁹ M SL-6), 2.3% for carotenoids (at 10⁻⁸ M SL-6), and 10.78% for total pigments (at 10⁻⁸ M SL-6) per gram biomass compared to the solvent control (DMSO). Higher doses of GR24 and SL-6 (10⁻⁷ M) inhibited microalgal growth, reducing cell density, biomass production, and pigment synthesis. The microalgal extracts acted as plant biostimulants, stimulating root and shoot elongation and proton pump functioning of mung seedlings in the presence and absence of salt stress. The extracts from SL-6 biostimulated C. sorokiniana were more active as plant biostimulants than the extracts from the non-stimulated C. sorokiniana.

This study aimed to evaluate the impact on Chlorella sorokiniana NIVA-CHL 176 growth and the plant biostimulant functions of the microalgal extract of the strigolactone mimic SL-6, in com-parison with the strigolactone analog GR24. Three molar SL-6 concentrations were tested: 10-7 M, 10-8 M, and 10-9 M, respectively. Five parameters of the microalgal growth were assessed: optical density, turbidity, biomass production, chlorophyll fluorescence, and pigment concentration. Results after 15 days of culturing revealed that the SL-6 treatments significantly enhanced bio-mass production, chlorophyll synthesis, and photosystem II activity. Treatment with SL-6 c3 (10-9 M) exhibited significant increases in chlorophyll a (27.55%), chlorophyll b (24.81%), carotenoids (12.31%), and total pigments (24.00%) compared to the solvent control (DMSO). Experimental treatment SL-6 c2 (10-8 M) followed next and recorded notable enhancements in chlorophyll a (25.80%), carotenoids (9.77%), and total pigments (20.08%). Conversely, higher doses of GR24 and SL-6 (10-7 M) inhibited the microalgal growth, reducing cell density, biomass production, and pigment synthesis. The microalgal extracts acted as a plant biostimulant stimulating root and shoot elongation and proton pump functioning in the presence and absence of salt stress. The extracts from SL-6 bio-stimulated C. sorokiniana NIVA-CHL 176 are more active as plant biostimulants.

This study represents an attempt toward the standardization of pulmonary NAMs and the development of a novel approach for toxicity testing of nanomaterials. Laboratory comparisons are challenging yet essential for identifying existing limitations and proposing potential solutions. Lung cells cultivated and exposed at the air-liquid interface (ALI) more accurately represent the physiology of human lungs and pulmonary exposure scenarios than submerged cell and exposure models. A triculture cell model system was used, consisting of human A549 lung epithelial cells and differentiated THP-1 macrophages on the apical side, with EA.hy926 endothelial cells on the basolateral side. The cells were exposed to silver nanoparticles NM-300K for 24 h. The model used here showed to be applicable for assessing the hazards of nanomaterials and chemicals, albeit with some limitations. Cellular viability was measured using the alamarBlue assay, DNA damage was assessed with the enzyme-modified comet assay, and the expression of 40 genes related to cell viability, inflammation, and DNA damage response was evaluated through RT² gene expression profiling. Despite harmonized protocols used in the two independent laboratories, however, some methodological challenges could affect the results, including sensitivity and reproducibility of the model.

Besides multiple benefits, high-residue farming systems have drawbacks: delayed development of the plant in early stages, nutrient availability, and enhanced risks for soil-borne diseases

Neuropsychiatric disorders are induced by various risk factors, including direct exposure to environmental chemicals. Arsenic exposure induces neurodegeneration and severe psychiatric disorders, but the molecular mechanisms by which brain damage is induced are not yet elucidated. Our aim is to better understand the molecular mechanisms of arsenic toxicity in the brain and to elucidate possible ways to prevent arsenic neurotoxicity, by reviewing significant experimental, bioinformatics, and cheminformatics studies. Brain damage induced by arsenic exposure is discussed taking in account: the correlation between neuropsychiatric disorders and the presence of arsenic and its derivatives in the brain; possible molecular mechanisms by which arsenic induces disturbances of cognitive and behavioral human functions; and arsenic influence during psychiatric treatments. Additionally, we present bioinformatics and cheminformatics tools used for studying brain toxicity of arsenic and its derivatives, new nanoparticles used as arsenic delivery systems into the human body, and experimental ways to prevent arsenic contamination by its removal from water. The main aim of the present paper is to correlate bioinformatics, cheminformatics, and experimental information on the molecular mechanism of cerebral damage induced by exposure to arsenic, and to elucidate more efficient methods used to reduce its toxicity in real groundwater.

The effects of long-term chronic exposure of human lung cells to multi-walled carbon nanotubes (MWCNT) and their impact upon cellular proteins and lipids were investigated. Since the lung is the major target organ, an in vitro normal bronchial epithelial cell line model was used. Additionally, to better mimic exposure to manufactured nanomaterials at occupational settings, cells were continuously exposed to two non-toxic and low doses of a MWCNT for 13-weeks. MWCNT-treatment increased ROS levels in cells without increasing oxidative DNA damage and resulted in differential expression of multiple anti- and pro-apoptotic proteins. The proteomic analysis of the MWCNT-exposed cells showed that among more than 5000 identified proteins; more than 200 were differentially expressed in the treated cells. Functional analyses revealed association of these differentially regulated proteins to cellular processes such as cell death and survival, cellular assembly, and organization. Similarly, shotgun lipidomic profiling revealed accumulation of multiple lipid classes. Our results indicate that long-term MWCNT-exposure of human normal lung cells at occupationally relevant low-doses may alter both the proteome and the lipidome profiles of the target epithelial cells in the lung.

In the present study, we address the important issue of whether B-cells protected from irradiation-induced cell death, may survive with elevated levels of DNA damage. If so, such cells would be at higher risk of gaining mutations and undergoing malignant transformation. We show that stimulation of B-cells with the TLR9 ligands CpG-oligodeoxynucleotides (CpG-ODN) prevents spontaneous and irradiation-induced death of normal peripheral blood B-cells, and of B-cells from patients diagnosed with Common variable immunodeficiency (CVID). The TLR9-mediated survival is enhanced by the vitamin A metabolite retinoic acid (RA). Importantly, neither stimulation of B-cells via TLR9 alone or with RA increases irradiation-induced DNA strand breaks and DNA damage responses such as activation of ATM and DNA-PKcs. We prove that elevated levels of γH2AX imposed by irradiation of stimulated B-cells is not due to induction of DNA double strand breaks, but merely reflects increased levels of total H2AX upon stimulation. Interestingly however, we unexpectedly find that TLR9 stimulation of B-cells induces low amounts of inactive p53, explained by transcriptional induction of TP53. Taken together, we show that enhanced survival of irradiated B-cells is not accompanied by elevated levels of DNA damage. Our results imply that TLR9-mediated activation of B-cells not only promotes cell survival, but may via p53 provide cells with a barrier against harmful consequences of enhanced activation and proliferation. As CVID-derived B-cells are more radiosensitive and prone to undergo apoptosis than normal B-cells, our data support treatment of CVID patients with CpG-ODN and RA.