Abstract
The production of free radicals is inevitably associated with metabolism and other enzymatic processes. Under physiological conditions, however, free radicals are effectively eliminated by numerous antioxidant mechanisms. Oxidative stress occurs due to an imbalance between the production and elimination of free radicals under pathological conditions. Oxidative stress is also associated with ageing. The brain is prone to oxidative damage because of its high metabolic activity and high vulnerability to ischemic damage. Oxidative stress, thus, plays a major role in the pathophysiology of both acute and chronic pathologies in the brain, such as stroke, traumatic brain injury or neurodegenerative diseases. The goal of this article is to summarize the basic concepts of oxidative stress and its significance in brain pathologies, as well as to discuss treatment strategies for dealing with oxidative stress in stroke.
Highlights
Apocynin has been shown to attenuate brain injury after experimental ischemic stroke and to reduce infarct size and levels of the apoptosis-inducing enzymes Bax and Bcl-2 [31,32]. It seems that apocynin functions as a nonspecific antioxidant, because it inhibits Rho kinase inhibitor, the p47phox subunit cannot migrate to the membrane and the NADPH oxidases (NOX) complex cannot assemble [33,34,35]
The lack of positive results in clinical trials does not necessarily disprove the important role of treating oxidative stress using antioxidants. These trials challenge us to better design antioxidant trials in the future and focus on using the best antioxidants at the right doses, in the right population and for the optimal duration. Both mitochondrial dysfunction and massive inflammatory response are strongly associated with cerebrovascular diseases
Oxidative stress plays a major role in the pathophysiology of stroke and other brain-related pathologies
Summary
Oxidative stress is described as a state of imbalance between the production of free radicals and their elimination by an organism’s anti-oxidative mechanisms. Electrons travel from one protein complex to the in the inner mitochondria membrane Intermediates in this reaction are, in nature, radicals [10]. At the end of the electron transport chain, the final electron acceptor is oxygen, and water is formed, which is not radical in nature [11] It is important these reactions take place from their beginnings to their ends. Antioxidant mechanisms kick in to scavenge or eliminate free radicals They do not have unlimited capacity and their recycling may be limited by the same factors as mitochondrial dysfunction [12]. The primary site for ROS generation is the mitochondria They can initiate cell death via cytochrome C release leading to activation of the intrinsic apoptotic pathway [24]. Oxidative stress plays an important role in cancer development [25,26]
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