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Published on: December 16, 2013
Mesoporous silica nanoparticles inhibit cellular respiration
Zhimin Tao1, Matthew P Morrow, Tewodros Asefa
1Department of Pediatrics, State University of New York, Upstate Medical University, 750 East Adams Street, Syracuse, New York 13210, USA.
Abstract:
We studied the effect of two types of mesoporous silica nanoparticles, MCM-41 and SBA-15, on mitochondrial O 2 consumption (respiration) in HL-60 (myeloid) cells, Jurkat (lymphoid) cells, and isolated mitochondria. SBA-15 inhibited cellular respiration at 25-500 microg/mL; the inhibition was concentration-dependent and time-dependent. The cellular ATP profile paralleled that of respiration. MCM-41 had no noticeable effect on respiration rate. In cells depleted of metabolic fuels, 50 microg/mL SBA-15 delayed the onset of glucose-supported respiration by 12 min and 200 microg/mL SBA-15 by 34 min; MCM-41 also delayed the onset of glucose-supported respiration. Neither SBA-15 nor MCM-41 affected cellular glutathione. Both nanoparticles inhibited respiration of isolated mitochondria and submitochondrial particles.
Insights
SBA-15 mesoporous silica nanoparticles inhibited cellular respiration and ATP production in a time- and concentration-dependent manner. MCM-41 showed minimal impact, suggesting differential nanoparticle toxicity.
Area of Science:
- Biomedical Engineering
- Nanotoxicology
- Cellular Respiration
Background:
- Mesoporous silica nanoparticles (MSNs) like MCM-41 and SBA-15 are widely investigated for biomedical applications.
- Understanding their potential cellular impacts, particularly on mitochondrial function, is crucial for safe application.
- Mitochondrial respiration is a key indicator of cellular health and energy production.
Purpose of the Study:
- To investigate the effects of MCM-41 and SBA-15 nanoparticles on mitochondrial O2 consumption (respiration) in different cell types and isolated mitochondria.
- To assess the impact of these nanoparticles on cellular ATP levels and metabolic fuel utilization.
- To determine the specificity of nanoparticle effects on cellular respiration.
Main Methods:
- Exposure of HL-60 (myeloid) and Jurkat (lymphoid) cells, along with isolated mitochondria, to varying concentrations of MCM-41 and SBA-15 nanoparticles.
- Measurement of cellular O2 consumption rates using respirometry.
- Analysis of cellular ATP levels and glutathione content.
- Assessment of respiration onset in metabolically deprived cells upon glucose addition.
Main Results:
- SBA-15 significantly inhibited cellular respiration in a concentration- and time-dependent manner, affecting both cell lines and isolated mitochondria.
- Cellular ATP levels mirrored the observed inhibition of respiration by SBA-15.
- MCM-41 demonstrated minimal to no significant impact on cellular respiration rates, although it delayed the onset of glucose-supported respiration.
- Neither nanoparticle affected cellular glutathione levels, but both inhibited isolated mitochondrial respiration.
Conclusions:
- SBA-15 exhibits significant mitochondrial toxicity, impacting cellular respiration and energy production.
- MCM-41 appears to have a lower toxicity profile concerning direct respiration inhibition, but potential indirect effects on metabolic pathways warrant further investigation.
- The differential effects highlight the importance of nanoparticle type and structure in determining cellular and mitochondrial responses.
