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氧化应激与焦虑症的发生关系:对可能的治疗干预的启示。

Association of oxidative stress to the genesis of anxiety: implications for possible therapeutic interventions.

机构信息

Pontifícia Universidade Católica do Rio de Janeiro, Rio de Janeiro, RJ, Brazil ; Institute of Chemical Sciences, University of Peshawar, Peshawar, Khyber Pakhtunkhwa, Pakistan.

Pontifícia Universidade Católica do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.

出版信息

Curr Neuropharmacol. 2014 Mar;12(2):120-39. doi: 10.2174/1570159X11666131120232135.

DOI:10.2174/1570159X11666131120232135
PMID:24669207
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3964744/
Abstract

Oxidative stress caused by reactive species, including reactive oxygen species, reactive nitrogen species, and unbound, adventitious metal ions (e.g., iron [Fe] and copper [Cu]), is an underlying cause of various neurodegenerative diseases. These reactive species are an inevitable by-product of cellular respiration or other metabolic processes that may cause the oxidation of lipids, nucleic acids, and proteins. Oxidative stress has recently been implicated in depression and anxiety-related disorders. Furthermore, the manifestation of anxiety in numerous psychiatric disorders, such as generalized anxiety disorder, depressive disorder, panic disorder, phobia, obsessive-compulsive disorder, and posttraumatic stress disorder, highlights the importance of studying the underlying biology of these disorders to gain a better understanding of the disease and to identify common biomarkers for these disorders. Most recently, the expression of glutathione reductase 1 and glyoxalase 1, which are genes involved in antioxidative metabolism, were reported to be correlated with anxiety-related phenotypes. This review focuses on direct and indirect evidence of the potential involvement of oxidative stress in the genesis of anxiety and discusses different opinions that exist in this field. Antioxidant therapeutic strategies are also discussed, highlighting the importance of oxidative stress in the etiology, incidence, progression, and prevention of psychiatric disorders.

摘要

活性物质引起的氧化应激,包括活性氧物种、活性氮物种和无束缚的、偶然的金属离子(如铁[Fe]和铜[Cu]),是各种神经退行性疾病的根本原因。这些活性物质是细胞呼吸或其他代谢过程的必然副产物,可能导致脂质、核酸和蛋白质的氧化。氧化应激最近与抑郁和焦虑相关障碍有关。此外,焦虑在许多精神疾病中的表现,如广泛性焦虑障碍、抑郁障碍、惊恐障碍、恐惧症、强迫症和创伤后应激障碍,突出了研究这些疾病的潜在生物学的重要性,以更好地了解疾病并确定这些疾病的共同生物标志物。最近,参与抗氧化代谢的谷胱甘肽还原酶 1 和甘油醛 3-磷酸脱氢酶 1 的表达与焦虑相关表型相关。这篇综述重点关注氧化应激在焦虑发生中的直接和间接证据,并讨论了该领域存在的不同观点。还讨论了抗氧化治疗策略,强调了氧化应激在精神疾病的病因、发病、进展和预防中的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7db8/3964744/93bd4a4c1654/CN-12-120_S3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7db8/3964744/7062cda05b3b/CN-12-120_S1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7db8/3964744/893a0f30779c/CN-12-120_S2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7db8/3964744/93bd4a4c1654/CN-12-120_S3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7db8/3964744/7062cda05b3b/CN-12-120_S1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7db8/3964744/893a0f30779c/CN-12-120_S2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7db8/3964744/93bd4a4c1654/CN-12-120_S3.jpg

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