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however, in specific genetic contexts, its abnormal splicing or functional inactivation may lead to insufficient intracellular iron accumulation, thereby limiting Fenton reaction efficiency and attenuating radiotherapy-induced lipid peroxidative damage (196).Conversely, overexpression of ACSL3, a member of the long-chain fatty acid-CoA ligase family, enhances the activation of polyunsaturated fatty acids (PUFAs) such as arachidonic acid (AA), promoting the synthesis of oxidation-sensitive phospholipids like AA-PE and significantly increasing membrane susceptibility to radiotherapy-induced lipid peroxidation (197)

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