Journal
BIOLOGICAL TRACE ELEMENT RESEARCH
Volume 199, Issue 6, Pages 2172-2181Publisher
SPRINGERNATURE
DOI: 10.1007/s12011-020-02323-4
Keywords
Cytotoxicity; Zinc oxide nanoparticles; DNA degradation; Reactive oxygen species
Funding
- Deanship of Scientific Research, King Abdulaziz University, Saudi Arabia [DF708-130-1441]
- King Abdulaziz University, Saudi Arabia
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This study investigated the anticancer properties of zinc oxide nanoparticles (ZnO-NPs) on human epidermoid carcinoma cells and found that ZnO-NPs induce apoptosis in A431 cells through DNA degradation and generation of reactive oxygen species via p53, bax/bcl-2, and caspase pathways.
Zinc oxide nanoparticles (ZnO-NPs) are used immensely in technology and medicine, but very less is known about toxicity mechanism to human epidermal cells. The objective of this study was to evaluate possible anticancer properties of ZnO-NPs on human epidermoid carcinoma cells using MTT assay, measurement of reactive oxygen species, DNA fragmentation, and nuclear condensation. ZnO-NPs were synthesized by sol-gel method using zinc acetate dihydrate, ethylene glycol, and 2-propyl alcohol. Numerous characterization techniques such as UV-visible spectroscopy, X-ray powder diffraction, transmission electron microscopy, and dynamic light scattering spectroscopy were used to confirm synthesis, purity, optical, and surface characteristics, size, shape, and distribution of ZnO-NPs. Our finding showed that ZnO-NPs considerably decreased cell viability of human epidermoid carcinoma A431 cells with a parallel increase in nuclear condensation and DNA fragmentation in a dose dependent manner. Moreover, real time PCR expression study showed that treatment of human epidermoid carcinoma cells with ZnO-NPs trigger increased expression of tumor suppressor gene p53, bax, and caspase-3 while downregulate antiapoptotic gene bcl-2. Thus ZnO-NPs induce apoptosis in A431 cells through DNA degradation and generation of reactive oxygen species via p53, bax/bcl-2, and caspase pathways.
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