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Selenium and L-carnitine protects from valproic acid-Induced oxidative stress and mitochondrial damages in rat cortical neurons
Drug and Chemical Toxicology ( IF 2.6 ) Pub Date : 2020-09-04 , DOI: 10.1080/01480545.2020.1810259
Ahmad Salimi 1 , Nasrin Alyan 2 , Nasim Akbari 2 , Zhaleh Jamali 3, 4 , Jalal Pourahmad 2
Affiliation  

Abstract

Oxidative stress and mitochondrial dysfunction have been associated with valproic acid (VPA) induced neurotoxicity. Mitochondria are vulnerable to oxidative damage and are also a major source of superoxide free radicals. Therefore, the need for mitochondrial protective and antioxidant agents for reducing valporic acid toxicity in central nerve system (CNS) is essential. In the present study, we investigated the potential beneficial effects of sodium selenite (SS) and L-carnitine (LC) against valproic acid -induced oxidative stress and mitochondrial dysfunction in isolated rat cortical neurons. Valproic acid (50, 100 and 200 µM) treatment caused a significant decrease in cellular viability, which was accompanied by increases in reactive oxygen species (ROS) generation, GSSG and GSH content, lipid peroxidation and lysosomal and mitochondrial damages. Sodium selenite (1 µM) and L-carnitine (1 mM) pretreatment attenuated valproic acid-induced decrease in cell viability. In addition, sodium selenite (1 µM) and L-carnitine (1 mM) pretreatment significantly protected against valproic acid-induced raise in oxidative stress, mitochondrial and lysosomal dysfunction, lipid peroxidation levels and depletion of GSH content. Our results in the current study provided insights into the protective mechanism by L-carnitine and sodium selenite, which is liked, to neuronal ROS generation and mitochondrial and lysosomal damages.



中文翻译:

硒和左旋肉碱可保护大鼠皮质神经元免受丙戊酸诱导的氧化应激和线粒体损伤

摘要

氧化应激和线粒体功能障碍与丙戊酸 (VPA) 诱导的神经毒性有关。线粒体易受氧化损伤,也是超氧自由基的主要来源。因此,需要线粒体保护剂和抗氧化剂来降低中枢神经系统 (CNS) 中丙戊酸的毒性是必不可少的。在本研究中,我们研究了亚硒酸钠 (SS) 和左旋肉碱 (LC) 对离体大鼠皮质神经元中丙戊酸诱导的氧化应激和线粒体功能障碍的潜在有益作用。丙戊酸(50、100 和 200 µM)处理导致细胞活力显着下降,同时伴随着活性氧 (ROS) 生成、GSSG 和 GSH 含量、脂质过氧化以及溶酶体和线粒体损伤的增加。亚硒酸钠 (1 µM) 和左旋肉碱 (1 mM) 预处理减弱了丙戊酸诱导的细胞活力下降。此外,亚硒酸钠 (1 µM) 和左旋肉碱 (1 mM) 预处理可显着防止丙戊酸诱导的氧化应激升高、线粒体和溶酶体功能障碍、脂质过氧化水平和 GSH 含量的消耗。我们在当前研究中的结果提供了对左旋肉碱和亚硒酸钠对神经元 ROS 产生以及线粒体和溶酶体损伤的保护机制的见解。线粒体和溶酶体功能障碍、脂质过氧化水平和 GSH 含量的消耗。我们在当前研究中的结果提供了对左旋肉碱和亚硒酸钠对神经元 ROS 产生以及线粒体和溶酶体损伤的保护机制的见解。线粒体和溶酶体功能障碍、脂质过氧化水平和 GSH 含量的消耗。我们在当前研究中的结果提供了对左旋肉碱和亚硒酸钠对神经元 ROS 产生以及线粒体和溶酶体损伤的保护机制的见解。

更新日期:2020-09-04
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