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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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100 nM MitoQ treatment resulted in differentiation as evidenced by an increase in neurite outgrowth 7 days after treatment, compared to the non-treated control

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