Cellular interactions of zinc oxide nanoparticles with human embryonic kidney (HEK 293) cells

• Published in: Colloids and surfaces, B, Biointerfaces B, Biointerfaces, 2017-09, Vol.157, p.182-190
• Main Authors: V G, Reshma, P V, Mohanan
• Format: Article
• Language: English
• Subjects: Apoptosis; Apoptosis - drug effects; Cell Survival - drug effects; Cytotoxicity; HEK293 Cells; Human embryonic kidney cells; Humans; Metal Nanoparticles - adverse effects; Metal Nanoparticles - chemistry; Nanoparticles - chemistry; Oxidative Stress - drug effects; Reactive oxygen species; Reactive Oxygen Species - metabolism; Zinc Oxide - adverse effects; Zinc Oxide - chemistry; ZnO nanoparticles
• ISSN: 0927-7765; 1873-4367
• DOI: 10.1016/j.colsurfb.2017.05.069

[Display omitted] •Characterization of ZnONPs.•Cellular morphological analysis of HEK cell.•Cytotoxicity and detection of ROS.•Cytoskeleton disruption.•Assessment of mitochondrial membrane potential. Zinc oxide nanoparticles (ZnO NPs) have potential biomedical, industrial and commercial applications. So they constantly come into contact with the body parts during applications. Safety concerns about ZnO NPs are increasing today and yet only few reports are available about their toxicity in kidney cells. It is very essential to analyze the toxicity on kidney because kidney plays a decisive role in nanoparticles excretion. Therefore, the present study focuses on the interaction of ZnO NPs with human embryonic kidney 293 (HEK 293) cells in vitro. The results showed that the cellular viability was much affected by ZnO NPs in a dose and time dependent manner. Oxidative stress increased the formation of reactive oxygen species (ROS), was found to be the prime mechanism of cytotoxicity. Formation of ROS eventually induced loss of mitochondrial membrane potential, lysosomal activity and nuclear condensation, which ultimately leads to apoptosis.