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Acrylamide induces mitochondrial dysfunction and apoptosis in BV-2 microglial cells
Zhigang Liu1, Ge Song2, Chen Zou2
1College of Food Science and Engineering, Northwest A&F University, Yangling, China; Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, USA.
Free Radical Biology & Medicine
|March 31, 2015
Summary
Acrylamide (ACR) exposure causes neurotoxicity by impairing mitochondrial function and redox balance, leading to apoptosis and inflammation. N-acetyl-L-cysteine (NAC) effectively reverses these harmful effects.
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Acrylamide (ACR) is a neurotoxin formed during high-temperature food processing.
- Microglia play crucial roles in neuroinflammation and neuronal health.
Purpose of the Study:
- To investigate the redox-dependent apoptotic and inflammatory responses of ACR in BV2 microglia.
- To elucidate the mechanisms underlying ACR-induced neurotoxicity.
Main Methods:
- BV2 cells were exposed to varying concentrations of ACR.
- Cell viability, apoptosis, mitochondrial function, and redox status were assessed.
- Key signaling pathways (Akt, JNK, p38, NFκB) and gene/protein expression were analyzed.
- The protective effects of N-acetyl-L-cysteine (NAC) were evaluated.
Main Results:
- ACR reduced cell viability and induced apoptosis in a dose-dependent manner.
- ACR impaired mitochondrial respiration, decreased membrane potential, and altered the Bcl-2/Bax ratio.
- ACR modulated redox-sensitive signaling, suppressed Akt, activated JNK/p38, and increased NFκB, iNOS, and nitric oxide.
- ACR depleted glutathione (GSH) and increased H2O2 formation.
- NAC treatment reversed ACR-induced mitochondrial dysfunction, redox imbalance, apoptosis, and inflammation.
Conclusions:
- ACR-induced mitochondrial dysfunction and oxidative stress are critical drivers of apoptosis and inflammation in microglia.
- NAC exhibits neuroprotective effects by restoring mitochondrial function and redox balance.
- Targeting mitochondrial pathways and redox status may offer therapeutic strategies against ACR toxicity.
