Oxidative Stress And Brain Ischemia

The adult human brain constitutes approximately 2% of total body weight but requires approximately 25% of the cardiac output. Because of its high oxygen consumption, the brain is especially vulnerable to oxidative stress. Furthermore, the brain's antioxidant capacity is very low due to low levels of enzymes, such as catalase and glutathione peroxidase, and high levels of iron and unsaturated fatty acids. Following ischemic injury, oxidative stress is a major cause of secondary injury through direct oxidant effects, as well as through activation of a variety of cell-death-signaling pathways (29). Especially in the setting of ischemia followed by reperfusion, pronounced oxidation occurs because large amounts of ROS in oxygenated blood enter the brain through recanalized vessels and through production in activated inflammatory cells. However, even in the absence of reperfusion, the ischemic brain can accumulate ROS. The mitochondrial respiratory chain is one of the main sites of cellular ROS generation, even under physiologic conditions; and, following ischemia, ROS generation further increases due to impaired respiration. ROS can directly react with all macromolecules of the brain cells, causing damage to protein, lipids, and DNA, and can oxidize low-molecular-weight reductants, such as glutathione, ascorbate, and alpha-tocopherol. ROS are also involved in the activation of inflammatory cells and various signaling cascades, thus underscoring their central role in mediating ischemic brain injury (Fig. 3).

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