Impairment of neuronal mitochondrial function by L-DOPA in the absence of oxygen-dependent auto-oxidation and oxidative cell damage.

ABSTRACT: L-3,4-Dihydroxyphenylalanin (L-DOPA or levodopa) is currently the most used drug to treat symptoms of Parkinson's disease (PD). After crossing the blood-brain barrier, it is enzymatically converted to dopamine by neuronal cells and restores depleted endogenous neurotransmitter levels. L-DOPA is prone to auto-oxidation and reactive intermediates of its degradation including reactive oxygen species (ROS) have been implicated in cellular damage. In this study, we investigated how oxygen tension effects L-DOPA stability. We applied oxygen tensions comparable to those in the mammalian brain and demonstrated that 2% oxygen almost completely stopped its auto-oxidation. L-DOPA even exerted a ROS scavenging function. Further mechanistic analysis indicated that L-DOPA reprogrammed mitochondrial meta

SUBMITTER: Hormann P 

PROVIDER: S-EPMC8257685 | biostudies-literature | 2021 Jun

REPOSITORIES: biostudies-literature