氧化应激
败血症
线粒体
活性氧
三磷酸腺苷
抗氧化剂
氧化磷酸化
器官功能障碍
细胞生物学
生物
化学
免疫学
生物化学
作者
Harsha Nagar,Shuyu Piao,Cuk‐Seong Kim
出处
期刊:Acute and Critical Care
[The Korean Society of Critical Care Medicine]
日期:2018-05-31
卷期号:33 (2): 65-72
被引量:74
标识
DOI:10.4266/acc.2018.00157
摘要
Mitochondria are considered the power house of the cell and are an essential part of the cellular infrastructure, serving as the primary site for adenosine triphosphate production via oxidative phosphorylation.These organelles also release reactive oxygen species (ROS), which are normal byproducts of metabolism at physiological levels; however, overproduction of ROS under pathophysiological conditions is considered part of a disease process, as in sepsis.The inflammatory response inherent in sepsis initiates changes in normal mitochondrial functions that may result in organ damage.There is a complex system of interacting antioxidant defenses that normally function to combat oxidative stress and prevent damage to the mitochondria.It is widely accepted that oxidative stress-mediated injury plays an important role in the development of organ failure; however, conclusive evidence of any beneficial effect of systemic antioxidant supplementation in patients with sepsis and organ dysfunction is lacking.Nevertheless, it has been suggested that antioxidant therapy delivered specifically to the mitochondria may be useful.
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