The role of NADPH oxidase in brain ischemia

نویسنده

  • Hai Chen
چکیده

Oxygen free radicals or oxidants that arise from molecular oxygen by successive single-electron reduction reactions, include the superoxide anion (O2), the hydrogen peroxide (H2O2), and hydroxyl radicals (·OH) (Chan 1996). Physiological levels of free radicals are needed for redox sensitive signal pathways, cell development and cell apoptosis (Chan 2001). During brain ischemia/reperfusion (I/R), oxygen is not well used; and robust oxygen radicals are generated in the brain. Excessive free radicals cause the cellular macromolecular damages of lipids, proteins, and nucleotide acids; thus, they play a crucial role in ischemic/reperfusion brain damage. NADPH oxidase (NOX) is a pro-oxidant enzyme that is expressed in various brain regions and its level is regulated by ischemia. This review is focused on the role of NOX in brain ischemia. Results from both in vivo and in vitro studies suggested that NOX plays a role in ischemic brain damage through producing oxygen radicals, contributing to excitotoxicity, and exacerbating post-ischemic inflammation process.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

O 22: Reactive Oxygen Species and Epilepsy

Seizure activity has been proposed to result in the generation of reactive oxygen species (ROS), which then contribute to seizure-induced neuronal damage and eventually cell death. Although the mechanisms of seizure-induced ROS generation are unclear, mitochondria and cellular calcium overload have been proposed to have a crucial role. We aim to determine the sources of seizure-induced ROS and ...

متن کامل

Spironolactone Inhibits NADPH Oxidase-Mediated Oxidative Stress and Dysregulation of the Endothelial NO Synthase in Human Endothelial Cells

Accumulating evidence indicates that aldosterone plays a critical role in the mediation of oxidative stress and vascular damage. NADPH oxidase has been recognized as a major source of oxidative stress in vasculature. However, the relation between NADPH oxidase in aldosterone-mediated oxidative stress in endothelial cells remains to be ascertained. The present study aimed to investigate the rel...

متن کامل

Spironolactone Inhibits NADPH Oxidase-Mediated Oxidative Stress and Dysregulation of the Endothelial NO Synthase in Human Endothelial Cells

Accumulating evidence indicates that aldosterone plays a critical role in the mediation of oxidative stress and vascular damage. NADPH oxidase has been recognized as a major source of oxidative stress in vasculature. However, the relation between NADPH oxidase in aldosterone-mediated oxidative stress in endothelial cells remains to be ascertained. The present study aimed to investigate the rel...

متن کامل

Apocynin in the Treatment of Ischemic Stroke

Apocynin has been used as an efficient inhibitor of the NADPH oxidase complex in experimental studies. NADPH oxidase was originally identified immune cells as playing an important microbicidal role. In cerebral ischemia, inflammation is increasingly being recognized as contributing negatively to neurological outcome, with NADPH-oxidase as an important source of superoxide. Recently, several for...

متن کامل

Potential therapeutic effect of pomegranate seed oil on ovarian ischemia/reperfusion injury in rats

Objective(s): The aim of this study is to determine the therapeutic effects of pomegranate seed oil, which is a powerful antioxidant and anti-inflammatory agent, on ovarian-ischemia and reperfusion injury in rats.Materials and Methods: Fifty-six  female albino Wistar rats were divided into 7 equal groups. Group 1; Sham Operation, Group 2; Ischemia, Group 3; Ischemia + Reperfusion, Group 4; Isch...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2009