Acrylamide Induces Abnormal mtDNA Expression by Causing Mitochondrial ROS Accumulation, Biogenesis, and Dynamics Disorders
TFAM
MFN2
Mitochondrial ROS
DOI:
10.1021/acs.jafc.1c02569
Publication Date:
2021-06-30T19:42:12Z
AUTHORS (6)
ABSTRACT
Acrylamide, a well-documented neurotoxicant, is commonly found as byproduct of the Maillard reaction in carbohydrate-rich foods. Numerous studies have indicated that acrylamide-induced apoptosis accompanied by mitochondrial dysfunction contributes to its neurotoxicity. However, mechanisms how acrylamide causes impairment not well understood. In this study, we observed destroyed redox balance, accumulated reactive oxygen species (ROS), damaged structures, and activated astrocytes following treatment. Furthermore, decreased expression biogenesis- dynamics-related genes, including PGC-1α, TFAM, Mfn2, Opa1, altered DNA (mtDNA)-encoded respiratory chain complexes, along with inhibited respiration. Pretreatment ROS scavenger mitoquinone dramatically restored expressions Opa1; protected structure; apoptosis. Further vivo experiments confirmed Opa1 rat brain tissues. These results revealed triggered accumulation interfere biogenesis dynamics, causing mtDNA damage finally resulting
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