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While LDL is mostly taken up by cells in target organs, excess LDL can deposit in the endothelial wall of blood vessels and initiate a cascade that ultimately contributes to the formation of atherosclerotic plaques [16, 17]

Although total antioxidant capacity (TAC) remained unchanged, the targeted reduction in specific oxidative stress markers appears to be meaningful clinical benefits, suggesting that the direct scavenging of lipid peroxides and free radicals, rather than systemic antioxidant enhancement, drives therapeutic efficacy [17,35]