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Abnormal iron metabolism is a significant trigger for ferroptosis, with iron-related proteins including transferrin receptor protein 1 (TfR1), ferritin (FTH and FTL), and iron export proteins playing essential roles in iron homeostasis

have shown that DENV-2 infection alters oxidative stress by increasing the levels of malondialdehyde (MDA), the end product of lipid peroxidation, and the oxidized glutathione/GSH ratio 126

This clearly suggested that the radioprotective functions of DSePA were through its incorporation into GPxs via increasing the bioavailable selenium pool rather than acting as a GPx mimic [61, 62, 84]