Oxidative Stress Neurons describes the pathological state where nerve cells are subjected to an overwhelming accumulation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), exceeding the neuron’s endogenous antioxidant capacity. This imbalance leads to molecular damage to DNA, lipids, and proteins, significantly impairing neuronal function and contributing to neuroinflammation and accelerated cell death. This condition is a primary mechanistic driver in the pathogenesis of numerous neurodegenerative disorders.
Origin
The term combines the biochemical concept of “oxidative stress,” referring to the imbalance between free radicals and antioxidants, with the specific cell type “neurons.” It emerged from free radical biology and neuroscience research, identifying the high metabolic rate and lipid-rich composition of neurons as factors making them particularly vulnerable to oxidative damage. Clinical interventions often focus on bolstering neuronal antioxidant defenses.
Mechanism
Neurons are highly susceptible to oxidative stress due to their high oxygen consumption, abundance of polyunsaturated fatty acids in their membranes, and relatively low levels of protective antioxidant enzymes compared to other cell types. Mitochondrial dysfunction is a major contributor, as damaged mitochondria produce excessive ROS as a byproduct of inefficient energy production. The resulting damage to mitochondrial DNA and cellular proteins disrupts synaptic transmission and ultimately triggers apoptotic pathways, leading to progressive neuronal loss.
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