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参与氧化还原反应的犬尿氨酸途径代谢物和酶。

Kynurenine pathway metabolites and enzymes involved in redox reactions.

作者信息

González Esquivel D, Ramírez-Ortega D, Pineda B, Castro N, Ríos C, Pérez de la Cruz V

机构信息

Departamento de Neuroquímica, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, S.S.A., México D.F. 14269, Mexico.

Laboratorio de Neuroinmunología, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, S.S.A., México D.F. 14269, Mexico.

出版信息

Neuropharmacology. 2017 Jan;112(Pt B):331-345. doi: 10.1016/j.neuropharm.2016.03.013. Epub 2016 Mar 10.

Abstract

Oxido-reduction reactions are a fundamental part of the life due to support many vital biological processes as cellular respiration and glucose oxidation. In the redox reactions, one substance transfers one or more electrons to another substance. An important electron carrier is the coenzyme NAD, which is involved in many metabolic pathways. De novo biosynthesis of NAD is through the kynurenine pathway, the major route of tryptophan catabolism, which is sensitive to redox environment and produces metabolites with redox capacity, able to alter biological functions that are controlled by redox-responsive signaling pathways. Kynurenine pathway metabolites have been implicated in the physiology process and in the physiopathology of many diseases; processes that also share others factors as dysregulation of calcium homeostasis, mitochondrial dysfunction, oxidative stress, inflammation and cell death, which impact the redox environment. This review examines in detail the available evidence in which kynurenine pathway metabolites participate in redox reactions and their effect on cellular redox homeostasis, since the knowledge of the main factors and mechanisms that lead to cell death in many neurodegenative disorders and other pathologies, such as mitochondrial dysfunction, oxidative stress and kynurenines imbalance, will allow to develop therapies using them as targets. This article is part of the Special Issue entitled 'The Kynurenine Pathway in Health and Disease'.

摘要

氧化还原反应是生命的基本组成部分,因为它支持许多重要的生物过程,如细胞呼吸和葡萄糖氧化。在氧化还原反应中,一种物质将一个或多个电子转移到另一种物质上。一种重要的电子载体是辅酶NAD,它参与许多代谢途径。NAD的从头生物合成是通过犬尿氨酸途径,这是色氨酸分解代谢的主要途径,该途径对氧化还原环境敏感,并产生具有氧化还原能力的代谢产物,能够改变由氧化还原反应信号通路控制的生物学功能。犬尿氨酸途径代谢产物与许多疾病的生理过程和病理生理有关;这些过程还与其他因素共同作用,如钙稳态失调、线粒体功能障碍、氧化应激、炎症和细胞死亡,这些都会影响氧化还原环境。这篇综述详细研究了犬尿氨酸途径代谢产物参与氧化还原反应的现有证据及其对细胞氧化还原稳态的影响,因为了解导致许多神经退行性疾病和其他病理状态(如线粒体功能障碍、氧化应激和犬尿氨酸失衡)中细胞死亡的主要因素和机制,将有助于开发以它们为靶点的治疗方法。本文是名为“健康与疾病中的犬尿氨酸途径”特刊的一部分。

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