Targeting Oxidative Stress for Neuroprotection.
Linseman DA
Antioxid Redox Signal 2008 Aug 20.
The generation of reactive oxygen species (ROS) and reactive nitrogen
species (RNS) leads to oxidative and/or nitrosative damage to cellular
proteins, lipids and DNA (a process collectively referred to here as
oxidative stress).
During ageing, oxidative stress increases due to an aberrant
generation of ROS/RNS and a gradual decline in cellular antioxidant
defense mechanisms.
Consequently, ageing and the associated increase in oxidative stress
are major risk factors for many neurodegenerative diseases. In
addition, various genetic mutations and environmental exposures can
sensitize individuals to oxidative stress and neurodegeneration.
Within the cell, mitochondria are a major source of oxidative stress.
However, additional intracellular sources of ROS and RNS exist, as
well as extracellular sources such as those resulting from
inflammation or exposure to toxins.
A significant body of literature indicates that ROS and/or RNS
resulting from mitochondrial dysfunction, neuroinflammation, or
toxicants are major factors in the oxidative stress-dependent neuronal
death that underlies various neurodegenerative disorders including
Parkinsons disease (PD), Alzheimers disease (AD), Huntingtons disease
(HD), amyotrophic lateral sclerosis (ALS), and many others (1, 8, 9,
16, 18).
Accordingly, the discovery of novel strategies to mitigate oxidative
stress is a principal focus of current therapeutic development
programs for neurodegenerative diseases.
Antioxidants & redox signaling [Antioxid Redox Signal]
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