Feitosa Chistiane Mendes, da Silva Oliveira George Laylson, do Nascimento Cavalcante Antonio, Morais Chaves Soane Kaline, Rai Mahendra
Department of Chemistry, University Federal of Piaui, Teresina, Brazil.
Department of Pharmacy, University Federal of Piaui, Teresina, Brazil.
Curr Clin Pharmacol. 2018;13(2):100-109. doi: 10.2174/1574884713666180301091612.
Oxidative stress is a major mechanism underlying the development of various neurodegenerative diseases (Alzheimer, Parkinson, Huntington and amyotrophic lateral sclerosis). Excessive formation of reactive oxygen species (ROS) and nitrogen (RNSs) can overburden the ability of the enzymatic antioxidant defense mechanisms (superoxide dismutase, catalase and glutathione reductase) and non-enzymatic (uric acid, ascorbic acid, α-tocopherol and reduced glutathione), causing the development of oxidative stress, and consequently, impairing the neuronal system cells by means of oxidative damage to a variety of important biological molecules such as lipids, DNA and proteins. Considering the importance of oxidative stress in neurodegenerative diseases, the present review aims to address the main parameters evaluated in in vitro studies on oxidative stress in different models of neurodegenerative diseases.The literary review was conducted through Pubmed, Science Direct, LILACS, Scielo and Google using following keywords: oxidative stress, neurodegenerative diseases and parameters of oxidative stress. We selected articles published between 2002 and 2017.The in vitro evaluation of the oxidative stress related parameters has provided a preliminary view about the pathogenesis of many neurodegenerative diseases (Alzheimer's, Parkinson's, Huntington's and Amyotrophic lateral sclerosis). In this way, it has demonstrated the mechanism of action of ROS/RNSs in these diseases by direct or indirect detection through several experimental procedures in vitro.
氧化应激是多种神经退行性疾病（阿尔茨海默病、帕金森病、亨廷顿病和肌萎缩侧索硬化症）发生发展的主要机制。活性氧（ROS）和活性氮（RNSs）的过度生成会使酶促抗氧化防御机制（超氧化物歧化酶、过氧化氢酶和谷胱甘肽还原酶）和非酶促抗氧化机制（尿酸、抗坏血酸、α-生育酚和还原型谷胱甘肽）的能力不堪重负，导致氧化应激的发生，进而通过对脂质、DNA和蛋白质等多种重要生物分子的氧化损伤来损害神经系统细胞。鉴于氧化应激在神经退行性疾病中的重要性，本综述旨在探讨在不同神经退行性疾病模型中进行的氧化应激体外研究中所评估的主要参数。通过使用以下关键词：氧化应激、神经退行性疾病和氧化应激参数，在PubMed、Science Direct、LILACS、Scielo和谷歌上进行了文献综述。我们选择了2002年至2017年发表的文章。对氧化应激相关参数的体外评估为许多神经退行性疾病（阿尔茨海默病、帕金森病、亨廷顿病和肌萎缩侧索硬化症）的发病机制提供了初步见解。通过体外的几种实验方法直接或间接检测，它已经证明了ROS/RNSs在这些疾病中的作用机制。
