| Literature DB >> 26937332 |
Ejaz Ahmed1, Tucker Donovan1, Lu Yujiao1, Quanguang Zhang1.
Abstract
There has been much evidence suggesting that reactive oxygen species (ROS) generated in mitochondria during cerebral ischemia play a major role in programming the senescence of organism. Antioxidants dealing with mitochondria slow down the appearance and progression of symptoms in cerebral ischemia and increase the life span of organisms. The mechanisms of mitochondrial targeted antioxidants, such as SKQ1, Coenzyme Q10, MitoQ, and Methylene blue, include increasing adenosine triphosphate (ATP) production, decreasing production of ROS and increasing antioxidant defenses, providing benefits in neuroprotection following cerebral ischemia. A number of studies have shown the neuroprotective role of these mitochondrial targeted antioxidants in cerebral ischemia. Here in this short review we have compiled the literature supporting consequences of mitochondrial dysfunction, and the protective role of mitochondrial targeted antioxidants.Entities:
Keywords: Antioxidants; Cerebral ischemia; Mitochondria; Reactive oxygen species
Year: 2015 PMID: 26937332 PMCID: PMC4771373 DOI: 10.21767/2171-6625.100017
Source DB: PubMed Journal: J Neurol Neurosci ISSN: 2171-6625