Eugene Baeg
Research Subjects
Eugene Baeg has a total of 2 co-authors. Here are the top co-authors by number of shared publications:
- Amornpun Sereemaspun
Center of Excellence in Nanomedicine Department of Anatomy Faculty of Medicine Chulalongkorn University Bangkok 10300 Thailand
1 shared publication - Kanidta Sooklert
Nanomedicine Research Unit, Department of Anatomy, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
1 shared publication
Latest Publications
- Open Access
- 12 October 2018
- Published by MDPI AG in Nanomaterials
- Vol. 8 (10) , 824
Copper Oxide Nanoparticles Cause a Dose-Dependent Toxicity via Inducing Reactive Oxygen Species in Drosophila
Copper oxide nanoparticles (CuONPs) have attracted considerable attention, because of their biocide potential and capability for optical imaging, however CuONPs were shown to be highly toxic in various experimental model systems. In this study, mechanism underlying CuONP-induced toxicity was investigated using Drosophila as an in vivo model. Upon oral route of administration, CuONPs accumulated in the body, and caused a dose-dependent decrease in egg-to-adult survivorship and a delay in development. In particular, transmission electron microscopy analysis revealed CuONPs were detected inside the intestinal epithelial cells and lumen. A drastic increase in apoptosis and reactive oxygen species was also observed in the gut exposed to CuONPs. Importantly, we found that inhibition of the transcription factor Nrf2 further enhances the toxicity caused by CuONPs. These observations suggest that CuONPs disrupt the gut homeostasis and that oxidative stress serves as one of the primary causes of CuONP-induced toxicity in Drosophila.
- 12 October 2018
- Published by MDPI AG in Nanomaterials
- Vol. 8 (10) , 824
Open AccessCopper Oxide Nanoparticles Cause a Dose-Dependent Toxicity via Inducing Reactive Oxygen Species in Drosophila
Copper oxide nanoparticles (CuONPs) have attracted considerable attention, because of their biocide potential and capability for optical imaging, however CuONPs were shown to be highly toxic in various experimental model systems. In this study, mechanism underlying CuONP-induced toxicity was investigated using Drosophila as an in vivo model. Upon oral route of administration, CuONPs accumulated in the body, and caused a dose-dependent decrease in egg-to-adult survivorship and a delay in development. In particular, transmission electron microscopy analysis revealed CuONPs were detected inside the intestinal epithelial cells and lumen. A drastic increase in apoptosis and reactive oxygen species was also observed in the gut exposed to CuONPs. Importantly, we found that inhibition of the transcription factor Nrf2 further enhances the toxicity caused by CuONPs. These observations suggest that CuONPs disrupt the gut homeostasis and that oxidative stress serves as one of the primary causes of CuONP-induced toxicity in Drosophila.