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Selenium nanoparticles induce autophagy mediated cell death in human keratinocytes
Shrikant Kirwale1, Venkatesh Pooladanda1, Sowjanya Thatikonda1
1Department of Regulatory Toxicology, National Institute of Pharmaceutical Education & Research (NIPER), Balanagar, Hyderabad, Telangana-500037, India.
Nanomedicine (London, England)
|July 30, 2019
Summary
Selenium nanoparticles (SeNPs) induce oxidative stress and cell death in skin cells. This occurs through increased autophagy, a cellular process involving lysosomes and autophagosomes, leading to programmed cell death in keratinocytes.
Area of Science:
- Nanomedicine
- Dermatology
- Cell Biology
Background:
- Selenium nanoparticles (SeNPs) show therapeutic potential for dermal disorders.
- Evaluating the toxicity of SeNPs in keratinocytes is crucial for understanding their safety and efficacy.
- The molecular mechanisms underlying SeNP-induced effects on skin cells require detailed investigation.
Purpose of the Study:
- To investigate the molecular mechanisms of cell death induced by SeNPs in human keratinocytes.
- To evaluate the role of oxidative stress and autophagy in SeNP-mediated toxicity.
- To determine the mode of cell death triggered by SeNPs in dermal cells.
Main Methods:
- Synthesis and characterization of SeNPs.
- Exposure of human keratinocytes to SeNPs.
- Assessment of oxidative stress markers.
- Evaluation of mitochondrial membrane potential.
- Analysis of autophagy markers, including acidic lysosomes and autophagosomes.
Main Results:
- SeNPs were synthesized and characterized for use in human keratinocytes.
- Exposure to SeNPs induced significant oxidative stress in keratinocytes.
- SeNPs triggered apoptotic cell death mediated by enhanced autophagy, evidenced by increased acidic lysosomes and autophagosomes.
Conclusions:
- SeNPs induce oxidative stress and apoptotic cell death in human keratinocytes.
- Autophagy plays a key role in the SeNP-induced cell death pathway.
- These findings provide insights into the molecular mechanisms of SeNP toxicity in dermal cells.
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