Acetaldehyde induces phosphorylation of dynamin-related protein 1 and mitochondrial dysfunction via elevating intracellular ROS and Ca²⁺ levels.

ABSTRACT: Excessive alcohol consumption impairs brain function and has been associated with an earlier onset of neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD). Acetaldehyde, the most toxic metabolite of alcohol, has been speculated to mediate the neurotoxicity induced by alcohol abuse. However, the precise mechanisms by which acetaldehyde induces neurotoxicity remain elusive. In this study, it was found that acetaldehyde treatment induced excessive mitochondrial fragmentation, impaired mitochondrial function and caused cytotoxicity in cortical neurons and SH-SY5Y cells. Further analyses showed that acetaldehyde induced the phosphorylation of mitochondrial fission related protein dynamin-related protein 1 (Drp1) at Ser616 and promoted its translocation to mit

SUBMITTER: Yan T 

PROVIDER: S-EPMC6879985 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature