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[5] Beyond its antioxidant properties, ALA may serve as an essential cofactor for mitochondrial enzymatic complexes (notably the -ketoacid dehydrogenases) involved in oxidative metabolism

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However, sustained excess ROS may lead to maladaptive hyperactivation of autophagy and, in some contexts, autophagy-associated cell death ( Therapeutically, the interface between autophagy and oxidative stress represents a promising target in MAFLD

the second is organic Se, which is actively absorbed by fish in the form of amino acids, combines with plasma protein to form SeMet

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This aligns with our research, underscoring the enhancement of mitochondrial function through mitophagy under hypoxic conditions