The aim of the study was to evaluate the effect of plasma acid on the uterine tissue of laboratory animals in vitro.Materials and methods. Treatment of dimethyl sulfoxide – water solution and water for injections with a spark discharge in air resulted in a decrease in pH, which contributed to generation of plasma acid in the solutions. We incubated uterine tissues in vitro in plasma acid at room temperature for 30 minutes. The treated tissues were examined histologically and immunohistochemically.Results. We showed that plasma acid had pronounced biological activity. Immunohistochemistry was used to show that, depending on the type of a solution, plasma acid altered generation of nitrosative damage products (3-NT) and oxidative DNA damage (8-OHdG) and modulated the number of cells with high proliferative potential (including CD133+ cells) and production of vascular endothelial growth factor (VEGF). These effects contributed to the general cytotoxicity of plasma acid solutions.Conclusion. During 30-minute exposure in vitro, plasma acid prepared from the dimethyl sulfoxide (DMSO) – water mixture exhibits various biological effects in uterine tissue samples obtained from experimental animals. Plasma-treated water exerts cytotoxic effects associated with oxidative DNA damage and promotes induction of pro-angiogenic activity in the uterine tissue. Plasma-treated DMSO does not have a cytotoxic effect. It inhibits cell proliferation, reducing the population of CD133+ cells and VEGF production in the tissue.
Brain development is a unique process characterized by mechanisms defined as neuroplasticity (synaptogenesis, synapse elimination, neurogenesis, and cerebral angiogenesis). Numerous neurodevelopmental disorders brain damage, and aging are manifested by neurological deficits that are caused by aberrant neuroplasticity. The presence of stem and progenitor cells in neurogenic niches of the brain is responsible for the formation of new neurons capable of integrating into preexisting synaptic assemblies. The determining factors for the cells within the neurogenic niche are the activity of the vascular scaffold and the availability of active regulatory molecules that establish the optimal microenvironment. It has been found that regulated intramembrane proteolysis plays an important role in the control of neurogenesis in brain neurogenic niches. Molecules generated by the activity of specific proteases can stimulate or suppress the activity of neural stem and progenitor cells, their proliferation and differentiation, migration and integration of newly formed neurons into synaptic networks. Local neoangiogenesis supports the processes of neurogenesis in neurogenic niches, which is guaranteed by the multivalent action of peptides formed from transmembrane proteins. Identification of new molecules regulating the neuroplasticity (neurogenesis and angiogenesis). i. e. enzymes, substrates, and products of intramembrane proteolysis, will ensure the development of protocols for detecting the neuroplasticity markers and targets for efficient pharmacological modulation.
The review focuses on molecular and biochemical mechanisms of nonspecific protection of respiratory epithelium. The authors provide a comprehensive analysis of up-to-date data on the activity of the lactoperoxidase system expressed on the surface of the respiratory epithelium which provides the generation of hypothiocyanate and hypoiodite in the presence of locally produced or inhaled hydrogen peroxide. Molecular mechanisms of production of active compounds with antiviral and antibacterial effects, expression profiles of enzymes, transporters and ion channels involved in the generation of hypothiocyanite and hypoiodate in the mucous membrane of the respiratory system in physiological and pathological conditions (inflammation) are discussed. In the context of antibacterial and antiviral defense special attention is paid to recent data confirming the effects of atmospheric air composition on the efficiency of hypothiocyanite and hypoiodate synthesis in the respiratory epithelium. The causes and outcomes of lactoperoxidase system impairment due to the action of atmospheric factors are discussed in the context of controlling the sensitivity of the epithelium to the action of bacterial agents and viruses. Restoration of the lactoperoxidase system activity can be achieved by application of pharmacological agents aimed to compensate for the lack of halides in tissues, and by the control of chemical composition of the inhaled air.
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