Oxidative stress mitigation is the physiological and therapeutic strategy aimed at reducing the cellular damage caused by an imbalance between the production of reactive oxygen species (ROS) and the cell’s capacity to detoxify these reactive intermediates. Excessive oxidative stress damages lipids, proteins, and DNA, accelerating cellular senescence and contributing to the pathology of numerous chronic diseases. Mitigation efforts focus on bolstering endogenous antioxidant defenses and reducing ROS generation.
Origin
The concept emerged from free radical biology in the mid-20th century, which established the link between oxygen metabolism, free radicals, and biological damage. The term “mitigation” reflects a clinical and preventative approach, acknowledging that complete elimination of ROS is neither possible nor desirable, as low levels serve as important signaling molecules. This area is central to contemporary longevity research.
Mechanism
The primary mechanism involves the upregulation of the cell’s endogenous antioxidant enzyme systems, including superoxide dismutase (SOD), catalase, and glutathione peroxidase. These enzymes work sequentially to neutralize ROS, converting highly reactive free radicals into less harmful molecules. Additionally, various nutritional and hormonal compounds act as non-enzymatic antioxidants, directly scavenging free radicals. The maintenance of optimal mitochondrial function and the regulation of cellular signaling pathways, such as Nrf2, are also key components in the overall process of stress mitigation.
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