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By curbing mitochondrial ROS generation at complexes I and II, riboflavin disrupts the vicious oxidative cycle, leading to diminished lipid peroxidation, preserved mitochondrial integrity, and reduced initiation of cell death pathwaysa convergent neuroprotective mechanism across diverse neuropathological contexts (35, 65)

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This article provides evidence for uncontrolled glucose consumption in cancer cells to generate reducing equivalents to detoxify ROS as a metabolic vulnerability for antitumour therapy

Moreover, genetic studies should be focused on an individual selenium intake in order to identify genegene and geneenvironment interactions responsible for stroke development in hypertensive subjects

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