AI Article Synopsis
- Oxidative stress occurs when there is an imbalance between harmful free radicals and the body's antioxidant defenses, leading to cellular damage and possible premature cell death.
- At low levels, antioxidants can mitigate the effects of reactive oxygen species (ROS), but excess ROS can cause inflammation and injury to cells.
- Recent research highlights the involvement of oxidative stress in various diseases, particularly in the brain, skin, and heart, with mitochondria serving as the primary source of ROS in cells.
Article Abstract
Oxidative stress is the resultant damage that arises due to redox imbalances, more specifically an increase in destructive free radicals and reduction in protection from antioxidants and the antioxidant defence pathways. Oxidation of lipids by reactive oxygen species (ROS) can damage cellular structures and result in premature cell death. At low levels, ROS-induced oxidative stress can be prevented through the action of antioxidants, however, when ROS are present in excess, inflammation and cytotoxicity eventually results leading to cellular oxidative stress damage. Increasing evidence for the role of oxidative stress in various diseases including neurological, dermatological, and cardiovascular diseases is now emerging. Mitochondria are the principal source (90%) of ROS in the cell, with superoxide radicals being generated when molecular oxygen is combined with free electrons. Given the key role of mitochondria in the generation of cellular oxidative stress it is worth considering this organelle and the process in more detail and to provide methods of intervention.
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