Oxidative stress tolerance is the physiological capacity of a cell or organism to withstand and effectively neutralize the damaging effects of reactive oxygen species (ROS) and free radicals generated during normal metabolism or in response to external stressors. High tolerance reflects a robust endogenous antioxidant defense system, which is crucial for protecting cellular components, including DNA, proteins, and lipids, from damage. A diminished tolerance is a hallmark of aging and chronic disease, indicating a compromised ability to maintain cellular integrity under metabolic load.
Origin
This term combines “oxidative stress,” the imbalance between free radical production and antioxidant defenses, with “tolerance,” the ability to endure or resist a harmful agent. It is a fundamental concept in redox biology and gerontology, where the cumulative effect of oxidative damage is recognized as a major contributor to biological aging.
Mechanism
Tolerance is maintained by a complex, multi-layered defense system, including enzymatic antioxidants like Superoxide Dismutase (SOD), Catalase, and Glutathione Peroxidase, as well as non-enzymatic antioxidants like Vitamin C and E. The Nrf2-Keap1 pathway is the master regulator, sensing oxidative stress and upregulating the expression of these protective enzymes. Robust tolerance relies on the continuous, efficient regeneration of these antioxidants and the prompt repair of any minor damage that does occur.
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