L-carnitine protects C2C12 cells against mitochondrial superoxide overproduction and cell death
L 肉毒碱保护 C2C12 房间免于 mitochondrial superoxide 生产过剩和房间死亡作者机构：Universitede Bourgogne-UFR SVTE Facultedes Science Gabriel
出 版 物：《World Journal of Biological Chemistry》 (世界生物化学杂志（英文版）（电子版）)
年 卷 期：2017年第8卷第1期
页 面：86-94页
学科分类：1001[医学-基础医学(可授医学、理学学位)] 100104[医学-病理学与病理生理学] 10[医学]
基 金：the Association Francaise contre les Myopathies for financial support
主 题：Superoxide anions Mitochondria Reactive Autophagy Muscle Carnitine Oxygen species Cell death
摘 要：AIM To identify and characterize the protective effect that L-carnitine exerted against an oxidative stress in C2C12 *** Myoblastic C2C12 cells were treated with menadione, a vitamin K analog that engenders oxidative stress, and the protective effect of L-carnitine(a nutrient involved in fatty acid metabolism and the control of the oxidative process), was assessed by monitoring various parameters related to the oxidative stress, autophagy and cell death. RESULTS Associated with its physiological function, a muscle cell metabolism is highly dependent on oxygen and may produce reactive oxygen species(ROS), especially under pathological conditions. High levels of ROS are known to induce injuries in cell structure as they interact at many levels in cell function. In C2C12 cells, a treatment with menadione induced a loss of transmembrane mitochondrial potential, an increase in mitochondrial production of ROS; it also induces autophagy and was able to provoke cell death. Pre-treatment of the cells with L-carnitine reduced ROS production, diminished autophagy and protected C2C12 cells against menadione-induced deleterious effects. CONCLUSION In conclusion, L-carnitine limits the oxidative stress in these cells and prevents cell death.
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