Publications by authors named "S M Korotkov"

Article Synopsis
  • - This review explores how oxidative stress from exposure to various heavy metals (like Ag, Hg, Cd, etc.) leads to apoptosis, a process of programmed cell death, affecting mitochondrial and cellular health.
  • - The mechanisms involved include activation of specific enzymes (caspases) and genes linked to apoptosis, as well as damage to mitochondria signified by changes in membrane potential and increased production of reactive oxygen species (ROS).
  • - Differences in thallium's toxic effects compared to other metals are highlighted, such as its unique interactions with cellular processes and metallothioneins, suggesting distinct pathways of toxicity and implications for human health.
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Lysine residues are essential in regulating enzymatic activity and the spatial structure maintenance of mitochondrial proteins and functional complexes. The most important parts of the mitochondrial permeability transition pore are F1F0 ATPase, the adenine nucleotide translocase (ANT), and the inorganic phosphate cotransporter. The ANT conformation play a significant role in the Tl-induced MPTP opening in the inner membrane of calcium-loaded rat liver mitochondria.

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Recent data have shown that the mitochondrial permeability transition pore (MPTP) is the complex of the Ca-modified adenine nucleotide translocase (ANT) and the Ca-modified ATP synthase. We found in a previous study that ANT conformational changes may be involved in Tl-induced MPTP opening in the inner membrane of Ca-loaded rat liver mitochondria. In this study, the effects of thiol-modifying agents (eosin-5-maleimide (EMA), fluorescein isothiocyanate (FITC), Cu(o-phenanthroline) (Cu(OP)), and embelin (Emb)), and MPTP inhibitors (ADP, cyclosporine A (CsA), n-ethylmaleimide (NEM), and trifluoperazine (TFP)) on MPTP opening were tested simultaneously with increases in swelling, membrane potential (ΔΨ) decline, decreases in state 3, 4, and 3U (2,4-dinitrophenol-uncoupled) respiration, and changes in the inner membrane free thiol group content.

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Over past few years, there has been a dramatic increase in studying physiological mechanisms of the activity of various signaling low-molecular molecules that directly or indirectly initiate adaptive changes in the cardiovascular system cells (CVSC) to hypoxia. These molecules include biologically active endogenous gases or gasotransmitters (HS, NO and CO) that influence on many cellular processes, including mitochondrial biogenesis, oxidative phosphorylation, K/Ca exchange, contractility of cardiomyocytes (CM) and vascular smooth muscle cells (VSMC) under conditions of oxygen deficiency. The present review focuses on the mechanistic role of the gasotransmitters (NO, HS, CO) in cardioprotection.

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This paper presents the results of a study of reversely switched dynistors (RSDs) with an operating voltage of 2.3 kV and a structure diameter of 12 mm in an unconventional mode, when they commutate current pulses with very short durations (a few microseconds). In this mode, we studied the dependence of the switching energy loss on the amount of charge that passes through the RSDs during the flow of the control current, which is reversed with respect to the main current.

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