The detrimental effect on skin structure and function resulting from an imbalance between the production of reactive oxygen species (ROS) and the skin’s intrinsic antioxidant defense capacity. This molecular stress leads to damage to cellular components, including DNA, proteins, and lipids, accelerating both intrinsic and extrinsic skin aging, particularly photoaging. It is a fundamental mechanism of environmental damage and cellular senescence in the integument.
Origin
The term combines “oxidative stress” (the molecular imbalance) and “dermal impact” (the resulting damage to the skin layer). This concept originated in biochemistry and free radical biology, later becoming a central tenet of modern dermatological research into aging and environmental pathology. It provides a chemical explanation for the degradation of the skin matrix.
Mechanism
Excessive ROS, generated by internal metabolism or external factors like UV radiation and pollution, directly attack and modify dermal components, leading to lipid peroxidation in cell membranes and the cross-linking and fragmentation of collagen and elastin fibers. Furthermore, oxidative stress activates pro-inflammatory signaling pathways and matrix metalloproteinases (MMPs) in fibroblasts, accelerating the breakdown of the extracellular matrix. The depletion of endogenous antioxidants, such as Vitamin E and glutathione, exacerbates this cumulative damage.
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