Free Radical Mitigation is a critical biological process and clinical strategy aimed at neutralizing or reducing the concentration of reactive oxygen species (ROS) and reactive nitrogen species (RNS) within the body to minimize oxidative stress and cellular damage. These highly reactive molecules, known as free radicals, are natural byproducts of cellular metabolism but, when in excess, damage lipids, proteins, and DNA, accelerating the aging process and contributing to chronic disease. Effective mitigation is paramount for preserving mitochondrial integrity and maintaining robust cellular function over time. This protective mechanism is a cornerstone of longevity medicine.
Origin
The concept is rooted in the Free Radical Theory of Aging, which posits that accumulated oxidative damage is a primary driver of senescence and age-related pathology. The clinical term “mitigation” emphasizes a proactive, therapeutic approach to supporting the body’s intrinsic antioxidant defense systems, moving beyond passive observation of oxidative markers. This strategy is central to protecting the delicate balance of redox signaling essential for cellular health.
Mechanism
Mitigation operates through a complex enzymatic and non-enzymatic antioxidant network, including key endogenous enzymes like superoxide dismutase (SOD), catalase, and glutathione peroxidase. These systems rapidly convert harmful free radicals into less reactive species. Exogenous nutritional support from antioxidants like vitamins C and E and polyphenols further augments this defense, acting as electron donors to stabilize the radicals. Hormonal signaling, particularly via the Nrf2 pathway, also plays a crucial role in upregulating the expression of these protective enzymes.
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