Abstract
The overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) is a common underlying mechanism of many neuropathologies, as they have been shown to damage various cellular components, including proteins, lipids and DNA. Free radicals, especially superoxide (O2 .-), and non-radicals, such as hydrogen peroxide (H2O2), can be generated in quantities large enough to overwhelm endogenous protective enzyme systems, such as superoxide dismutase (SOD) and reduced glutathione (GSH). Here we review the mechanisms of ROS and RNS production, and their roles in ischemia, traumatic brain injury and aging. In particular, we discuss several acute and chronic pharmacological therapies that have been extensively studied in order to reduce ROS/RNS loads in cells and the subsequent oxidative stress, so-called “free-radical scavengers.” Although the overall aim has been to counteract the detrimental effects of ROS/RNS in these pathologies, success has been limited, especially in human clinical studies. This review highlights some of the recent successes and failures in animal and human studies by attempting to link a compounds chemical structure with its efficacy as a free radical scavenger. In particular, we demonstrate how antioxidants derived from natural products, as well as long-term dietary alterations, may prove to be effective scavengers of ROS and RNS.
Keywords: Anthocyanins, natural products, NXY-059, oxidative stress, oxyresveratrol, reactive nitrogen species, reactive oxygen species, superoxide
Current Medicinal Chemistry
Title: Antioxidants and Free Radical Scavengers for the Treatment Of Stroke, Traumatic Brain Injury and Aging
Volume: 15 Issue: 4
Author(s): J. T. Weber, J. E. Slemmer, J. J. Shacka and M. I. Sweeney
Affiliation:
Keywords: Anthocyanins, natural products, NXY-059, oxidative stress, oxyresveratrol, reactive nitrogen species, reactive oxygen species, superoxide
Abstract: The overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) is a common underlying mechanism of many neuropathologies, as they have been shown to damage various cellular components, including proteins, lipids and DNA. Free radicals, especially superoxide (O2 .-), and non-radicals, such as hydrogen peroxide (H2O2), can be generated in quantities large enough to overwhelm endogenous protective enzyme systems, such as superoxide dismutase (SOD) and reduced glutathione (GSH). Here we review the mechanisms of ROS and RNS production, and their roles in ischemia, traumatic brain injury and aging. In particular, we discuss several acute and chronic pharmacological therapies that have been extensively studied in order to reduce ROS/RNS loads in cells and the subsequent oxidative stress, so-called “free-radical scavengers.” Although the overall aim has been to counteract the detrimental effects of ROS/RNS in these pathologies, success has been limited, especially in human clinical studies. This review highlights some of the recent successes and failures in animal and human studies by attempting to link a compounds chemical structure with its efficacy as a free radical scavenger. In particular, we demonstrate how antioxidants derived from natural products, as well as long-term dietary alterations, may prove to be effective scavengers of ROS and RNS.
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Cite this article as:
Weber T. J., Slemmer E. J., Shacka J. J. and Sweeney I. M., Antioxidants and Free Radical Scavengers for the Treatment Of Stroke, Traumatic Brain Injury and Aging, Current Medicinal Chemistry 2008; 15 (4) . https://dx.doi.org/10.2174/092986708783497337
DOI https://dx.doi.org/10.2174/092986708783497337 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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