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Oxidative damage is the main factor affecting RBC storage lesion which is caused by free radicals.[1] Free radicals damage the RBC products by lipid, protein oxidation and oxidative loss with changes in the structure of the RBCs membrane leads to an increase in the accumulation of band-3 protein, lipid oxidationΩ and apoptotic changes in the last weeks of storage
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These advanced in vitro systems are crucial for validating the complex interplay between genetic risk, viral mechanisms, and Ξ² cell pathology identified in epidemiological studies, moving beyond correlational data to establish a causal mechanism
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