Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/31508
Title: The role of oxidative stress in anxiety disorder: cause or consequence?
Authors: Fedoce, Alessandra das Graças
Ferreira, Frederico
Bota, Robert G.
Bonet-Costa, Vicent
Sun, Patrick Y.
Davies, Kelvin J. A.
Affilliation: The University of Southern California. Leonard Davis School of Gerontology of the Ethel Percy. Andrus Gerontology Center. Los Angeles, CA, USA.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa sobre o Timo. Rio de Janeiro, RJ, Brasil.
University of California Irvine. Department of Psychiatry. Orange, CA, USA.
The University of Southern California. Leonard Davis School of Gerontology of the Ethel Percy. Andrus Gerontology Center. Los Angeles, CA, USA.
The University of Southern California. Leonard Davis School of Gerontology of the Ethel Percy. Andrus Gerontology Center. Los Angeles, CA, USA.
The University of Southern California. Leonard Davis School of Gerontology of the Ethel Percy. Andrus Gerontology Center. Los Angeles, CA, USA / The University of Southern California. Dornsife College of Letters, Arts, & Sciences. Department of Biological Sciences, Los Angeles, CA, USA.
Abstract: Anxiety disorders are the most common mental illness in the USA affecting 18% of the population. The cause(s) of anxiety disorders is/are not completely clear, and research in the neurobiology of anxiety at the molecular level is still rather limited. Although mounting clinical and preclinical evidence now indicates that oxidative stress may be a major component of anxiety pathology, whether oxidative stress is the cause or consequence remains elusive. Studies conducted over the past few years suggest that anxiety disorders may be characterised by lowered antioxidant defences and increased oxidative damage to proteins, lipids, and nucleic acids. In particular, oxidative modifications to proteins have actually been proposed as a potential factor in the onset and progression of several psychiatric disorders, including anxiety and depressive disorders. Oxidised proteins are normally degraded by the proteasome proteolytic complex in the cell cytoplasm, nucleus, and endoplasmic reticulum. The Lon protease performs a similar protective function inside mitochondria. Impairment of the proteasome and/or the Lon protease results in the accumulation of toxic oxidised proteins in the brain, which can cause severe neuronal trauma. Recent evidence points to possible proteolytic dysfunction and accumulation of damaged, oxidised proteins as factors that may determine the appearance and severity of psychotic symptoms in mood disorders. Thus, critical interactions between oxidative stress, proteasome, and the Lon protease may provide keys to the molecular mechanisms involved in emotional regulation, and may also be of great help in designing and screening novel anxiolytics and antidepressants.
Keywords: Antioxidants
Anxiety disorder
Inflammation
Lon protease
Nrf2
oxidative stress
proteasome
psychiatric disorders
keywords: Antioxidantes
Transtorno de ansiedade
Inflamação
Estresse oxidativo
Distúrbios psiquiátricos
Proteassoma
Issue Date: 2018
Publisher: Taylor & Francis
Citation: FEDOCE, Alessandra das Graças et al. The role of oxidative stress in anxiety disorder: cause or consequence?. Free Radical Research, v. 52, n. 7, p. 737-750, 2018.
DOI: 10.1080/10715762.2018.1475733
ISSN: 1071-5762
Copyright: restricted access
Appears in Collections:IOC - Artigos de Periódicos

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