Publication | Open Access

On the neurotoxicity mechanism of leukoaminochrome o-semiquinone radical derived from dopamine oxidation: mitochondria damage, necrosis, and hydroxyl radical formation

OxysterolMedicineLipid PeroxidationCell DeathNeuroprotectionNeuroscienceReactive Oxygen SpeciePharmacologyDopamine OxidationRedox BiologyMitochondria DamageHydroxyl Radical FormationOxidative Stress