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Updated: Mar 8, 2026
Microglia as a Surrogate Biosensor to Determine Nanoparticle Neurotoxicity
Published on: October 25, 2016
Mitochondrial dysfunction, oxidative stress and apoptotic induction in microglial BV-2 cells treated with sodium
Wafa Kharroubi1, Samia Haj Ahmed1, Thomas Nury2
1Univ. Bourgogne Franche-Comté Laboratory Bio-PeroxIL, Biochemistry of the Peroxisome, Inflammation and Lipid Metabolism EA7270/INSERM, Faculty of Sciences Gabriel, Dijon 21000, France; Laboratory of Nutrition-Functional Foods and Vascular Diseases, Faculty of Medicine, University of Monastir, Monastir 5019, Tunisia.
Abstract:
The treatment of microglial BV-2 cells with sodium arsenate (As(V): 0.1-400μmol/L - 48hr) induces a dose-dependent response. The neurotoxic effects of high concentrations of As(V) (100, 200 and 400μmol/L) are characterized by increased levels of mitochondrial complexes I, II, and IV followed by increased superoxide anion generation. Moreover, As(V) triggers an apoptotic mode of cell death, demonstrated by an apoptotic SubG1 peak, associated with an alteration of plasma membrane integrity. There is also a decrease in transmembrane mitochondrial potential and mitochondrial adenosine triphosphate ATP. It is therefore tempting to speculate that As(V) triggers mitochondrial dysfunction, which may lead to defective oxidative phosphorylation subsequently causing mitochondrial oxidative damage, which in turn induces an apoptotic mode of cell death.
Insights
Sodium arsenate (As(V)) causes dose-dependent neurotoxicity in microglial cells. High concentrations induce mitochondrial dysfunction, oxidative stress, and apoptosis, impacting cell integrity and ATP levels.
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Microglial cells play crucial roles in brain immunity and inflammation.
- Arsenic exposure is a significant environmental health concern with known neurotoxic potential.
Purpose of the Study:
- To investigate the dose-dependent neurotoxic effects of sodium arsenate (As(V)) on microglial BV-2 cells.
- To elucidate the mechanisms underlying As(V)-induced cell death, focusing on mitochondrial dysfunction and oxidative stress.
Main Methods:
- Treatment of BV-2 cells with varying concentrations of sodium arsenate (0.1-400 μmol/L) for 48 hours.
- Assessment of mitochondrial complex activity (I, II, IV), superoxide anion generation, and plasma membrane integrity.
- Flow cytometry analysis to detect apoptotic SubG1 peak, mitochondrial membrane potential, and ATP levels.
Main Results:
- As(V) induced a dose-dependent response in BV-2 cells.
- High As(V) concentrations (100-400 μmol/L) increased mitochondrial complexes I, II, and IV, leading to elevated superoxide anion generation.
- As(V) triggered apoptosis, evidenced by a SubG1 peak, altered plasma membrane integrity, decreased mitochondrial membrane potential, and reduced ATP production.
Conclusions:
- Sodium arsenate induces significant mitochondrial dysfunction in microglial cells.
- This dysfunction involves impaired oxidative phosphorylation and increased oxidative damage, ultimately leading to apoptosis.
- As(V) poses a neurotoxic risk by compromising microglial cell viability through mitochondrial pathways.
