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Malondialdehyde (MDA) is a highly reactive three-carbon dialdehyde that serves as a primary biomarker for lipid peroxidation and oxidative stress (Ayala et al., 2014). It is generated through the degradation of polyunsaturated fatty acids by reactive oxygen species or via enzymatic pathways involving cyclooxygenases (PubChem CID 10964). MDA is chemically potent, forming covalent adducts with DNA bases, primarily deoxyguanosine, and protein residues like lysine (Del Rio et al., 2005). These adducts lead to mutations, genomic instability, and impaired enzymatic activity, contributing to cellular dysfunction and death. The pathways associated with MDA-induced damage are central to the progression of various chronic diseases, including atherosclerosis, where MDA-modified LDL promotes foam cell formation, and neurodegeneration (Zarkovic, 2003). Although MDA is not a classical therapeutic target like a receptor, it is a critical focal point for antioxidant therapies and carbonyl-scavenging drugs, such as hydralazine, designed to mitigate oxidative tissue injury (Burcham et al., 2002).
Scavenging of reactive carbonyl species and inhibition of lipid peroxidation to prevent covalent modification of biomolecules.
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