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The antioxidant enzymes and glutathione system represent a complex network of proteins and small molecules dedicated to maintaining cellular redox homeostasis and protecting cells from oxidative damage. Key enzymatic components include Superoxide dismutase (SOD), which dismutates superoxide radicals; Catalase (CAT), which decomposes hydrogen peroxide; and the Glutathione peroxidase (GPx) family, which reduces hydroperoxides using glutathione as a cofactor (Source: PMID: 24513455). The system is centered around the tripeptide glutathione (GSH), the most abundant endogenous antioxidant, which also participates in the detoxification of xenobiotics via Glutathione S-transferases (GSTs). Dysregulation of this system leads to oxidative stress, a state implicated in the pathogenesis of neurodegenerative disorders like Parkinson's disease, cardiovascular diseases, and various cancers (Source: NIH StatPearls). Pharmacological intervention often focuses on Nrf2 activators to upregulate the entire suite of antioxidant genes or the use of glutathione precursors like N-acetylcysteine to restore cellular defense mechanisms during acute injury or chronic inflammation (Source: PubChem).
Drugs targeting this system typically act by replenishing glutathione precursors, acting as enzymatic mimetics (e.g., glutathione peroxidase mimetics), or inducing the expression of antioxidant enzymes through the activation of the Nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway (Source: PMID: 23202305, NIH StatPearls).
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