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Copper and CuNPs have the ability to stimulate apoptosis by caspase-dependent and independent pathways through induction of pro-apoptotic protein (Bax) and suppression of anti-apoptotic protein (Bcl-2) [66, 90, 96], while chrysin activates apoptosis through intrinsic pathways of apoptosis in view of p53 and Bak, caspase-9 and caspase-3 enhancement, and Bcl2 downregulation [96]

S1P is a bioactive sphingolipid molecule that regulates various cellular functions, including cell survival, differentiation, migration, proliferation, and immune responses, through its binding to five G protein-coupled receptors (S1PR1 to S1PR5) [69]

This protein can create an iron-overloaded environment and lay the foundation for the occurrence of cellular ferroptosis