Free radical damage, clinically termed oxidative stress, describes the cellular and molecular injury caused by highly reactive molecules possessing unpaired electrons. These unstable oxygen species, or reactive oxygen species (ROS), indiscriminately attack vital cellular components including DNA, proteins, and lipid membranes. Uncontrolled accumulation of this damage accelerates cellular senescence and contributes significantly to the pathophysiology of age-related diseases and endocrine dysfunction. Managing this stress is paramount for longevity and systemic health.
Origin
The concept originated from the Free Radical Theory of Aging, proposed in the mid-20th century, which posited that aging is primarily a consequence of cumulative oxidative damage over time. The term ‘Free Radical’ derives from chemistry, denoting any atom or molecule with an unpaired valence electron, making it highly unstable and eager to react with surrounding molecules. In biology, this concept is central to understanding the intrinsic costs of aerobic metabolism.
Mechanism
The primary mechanism involves the free radical species attempting to achieve stability by stealing an electron from a nearby stable molecule, thus initiating a chain reaction. When this chain reaction targets cell membranes, it causes lipid peroxidation, compromising cellular integrity. Damage to mitochondrial DNA impairs energy production, creating a vicious cycle of increased ROS generation and further cellular decline. The body’s natural defense involves endogenous antioxidant enzymes like superoxide dismutase and glutathione, which neutralize these species.
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