34 research outputs found

    Pathophysiological Mechanisms of Antipsychotic-Induced Parkinsonism

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    Among neurological adverse reactions in patients with schizophrenia treated with antipsychotics (APs), drug-induced parkinsonism (DIP) is the most common motility disorder caused by drugs affecting dopamine receptors. One of the causes of DIP is the disruption of neurotransmitter interactions that regulate the signaling pathways of the dopaminergic, cholinergic, GABAergic, adenosinergic, endocannabinoid, and other neurotransmitter systems. Presently, the development mechanisms remain poorly understood despite the presence of the considered theories of DIP pathogenesis

    Polyamine Metabolism and Oxidative Protein Folding in the ER as ROS-Producing Systems Neglected in Virology

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    Reactive oxygen species (ROS) are produced in various cell compartments by an array of enzymes and processes. An excess of ROS production can be hazardous for normal cell functioning, whereas at normal levels, ROS act as vital regulators of many signal transduction pathways and transcription factors. ROS production is affected by a wide range of viruses. However, to date, the impact of viral infections has been studied only in respect to selected ROS-generating enzymes. The role of several ROS-generating and-scavenging enzymes or cellular systems in viral infections has never been addressed. In this review, we focus on the roles of biogenic polyamines and oxidative protein folding in the endoplasmic reticulum (ER) and their interplay with viruses. Polyamines act as ROS scavengers, however, their catabolism is accompanied by H 2 O 2 production. Hydrogen peroxide is also produced during oxidative protein folding, with ER oxidoreductin 1 (Ero1) being a major source of oxidative equivalents. In addition, Ero1 controls Ca 2+ efflux from the ER in response to e.g., ER stress. Here, we briefly summarize the current knowledge on the physiological roles of biogenic polyamines and the role of Ero1 at the ER, and present available data on their interplay with viral infections

    Polyamine Metabolism and Oxidative Protein Folding in the ER as ROS-Producing Systems Neglected in Virology

    No full text
    Reactive oxygen species (ROS) are produced in various cell compartments by an array of enzymes and processes. An excess of ROS production can be hazardous for normal cell functioning, whereas at normal levels, ROS act as vital regulators of many signal transduction pathways and transcription factors. ROS production is affected by a wide range of viruses. However, to date, the impact of viral infections has been studied only in respect to selected ROS-generating enzymes. The role of several ROS-generating and -scavenging enzymes or cellular systems in viral infections has never been addressed. In this review, we focus on the roles of biogenic polyamines and oxidative protein folding in the endoplasmic reticulum (ER) and their interplay with viruses. Polyamines act as ROS scavengers, however, their catabolism is accompanied by H2O2 production. Hydrogen peroxide is also produced during oxidative protein folding, with ER oxidoreductin 1 (Ero1) being a major source of oxidative equivalents. In addition, Ero1 controls Ca2+ efflux from the ER in response to e.g., ER stress. Here, we briefly summarize the current knowledge on the physiological roles of biogenic polyamines and the role of Ero1 at the ER, and present available data on their interplay with viral infections

    Blood and Urinary Biomarkers of Antipsychotic-Induced Metabolic Syndrome

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    Metabolic syndrome (MetS) is a clustering of at least three of the following five medical conditions: abdominal obesity, high blood pressure, high blood sugar, high serum triglycerides, and low serum high-density lipoprotein (HDL). Antipsychotic (AP)-induced MetS (AIMetS) is the most common adverse drug reaction (ADR) of psychiatric pharmacotherapy. Herein, we review the results of studies of blood (serum and plasma) and urinary biomarkers as predictors of AIMetS in patients with schizophrenia (Sch). We reviewed 1440 studies examining 38 blood and 19 urinary metabolic biomarkers, including urinary indicators involved in the development of AIMetS. Among the results, only positive associations were revealed. However, at present, it should be recognized that there is no consensus on the role of any particular urinary biomarker of AIMetS. Evaluation of urinary biomarkers of the development of MetS and AIMetS, as one of the most common concomitant pathological conditions in the treatment of patients with psychiatric disorders, may provide a key to the development of strategies for personalized prevention and treatment of the condition, which is considered a complication of AP therapy for Sch in clinical practice

    Effect of Chitin Nanofibrils on Biocompatibility and Bioactivity of the Chitosan-Based Composite Film Matrix Intended for Tissue Engineering

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    This paper discusses the mechanical and physicochemical properties of film matrices based on chitosan, as well as the possibility of optimizing these properties by adding chitin nanofibrils. It is shown that with the introduction of chitin nanofibrils as a filler, the mechanical stability of the composite materials increases. By varying the concentration of chitin nanofibrils, it is possible to obtain a spectrum of samples with different bioactive properties for the growth of human dermal fibroblasts. Film matrices based on the nanocomposite of chitosan and 5 wt % chitin nanofibrils have an optimal balance of mechanical and physicochemical properties and bioactivity in relation to the culture of human dermal fibroblasts

    Design of Anode Materials for IT SOFC:Effect of Complex Oxide Promoters and Pt Group Metals on Activity and Stability in Methane Steam Reforming of Ni/YSZ (ScSZ) Cermets

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    Ni/YSZ or Ni/ScCeSZ cermets were promoted by up to 10 wt % of fluoritelike (Pr-Ce-Zr- O, La-Ce-Zr-O, and Ce-Zr-O) or perovskitelike (La-Pr-Mn-Cr-O) oxides and small (up to 1.4 wt %) amounts of Pt group metals (Pd, Pt, or Ru). Reactivity of samples, their lattice oxygen mobility, and their ability to activate methane were characterized by temperature-programed reduction by CH4. The catalytic properties of these samples in methane steam reforming were studied at 500-850 degrees C and short contact times (10 ms) in feeds with 8 mol % of CH4 and steam/methane ratio of 1: 3. Oxide promoters ensure stable performance of cermets in stoichiometric feeds at T &gt; 650 degrees C by suppressing carbon deposition. Copromotion with precious metals enhances performance in the intermediate temperature (450-600 degrees C) range due to more efficient activation of methane. Factors determining specificity of these cermet materials' performance (chemical composition, microstructure, oxygen mobility in oxides, interaction between components, and reaction media effect) are considered. The most promising systems for practical application are Pt/Pr-Ce-Zr-O/Ni/YSZ and Ru/La-Pr-Mn-Cr-O/Ni/YSZ cermets demonstrating a high performance in the intermediate temperature range under broad variation in steam/CH4 ratio. [DOI: 10.1115/1.3117255]</p

    Hepatitis Delta Virus Antigens Trigger Oxidative Stress, Activate Antioxidant Nrf2/ARE Pathway, and Induce Unfolded Protein Response

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    Hepatitis delta virus (HDV) is a viroid-like satellite that may co-infect individuals together with hepatitis B virus (HBV), as well as cause superinfection by infecting patients with chronic hepatitis B (CHB). Being a defective virus, HDV requires HBV structural proteins for virion production. Although the virus encodes just two forms of its single antigen, it enhances the progression of liver disease to cirrhosis in CHB patients and increases the incidence of hepatocellular carcinoma. HDV pathogenesis so far has been attributed to virus-induced humoral and cellular immune responses, while other factors have been neglected. Here, we evaluated the impact of the virus on the redox status of hepatocytes, as oxidative stress is believed to contribute to the pathogenesis of various viruses, including HBV and hepatitis C virus (HCV). We show that the overexpression of large HDV antigen (L-HDAg) or autonomous replication of the viral genome in cells leads to increased production of reactive oxygen species (ROS). It also leads to the upregulated expression of NADPH oxidases 1 and 4, cytochrome P450 2E1, and ER oxidoreductin 1α, which have previously been shown to mediate oxidative stress induced by HCV. Both HDV antigens also activated the Nrf2/ARE pathway, which controls the expression of a spectrum of antioxidant enzymes. Finally, HDV and its large antigen also induced endoplasmic reticulum (ER) stress and the concomitant unfolded protein response (UPR). In conclusion, HDV may enhance oxidative and ER stress induced by HBV, thus aggravating HBV-associated pathologies, including inflammation, liver fibrosis, and the development of cirrhosis and hepatocellular carcinoma
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