TOXICITY OF METAL OXIDE NANOPARTICLES TO CAENORHABDITIS ELEGANS

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dc.contributor.advisorPan, Xiaopingen_US
dc.contributor.authorArmstrong, Michael Christoheren_US
dc.contributor.departmentBiologyen_US
dc.date.accessioned2012-05-20T15:20:24Z
dc.date.available2014-05-31T12:06:21Z
dc.date.issued2012en_US
dc.description.abstractThe increase in manufacturing and use of nanoparticles is expected to elevate levels of exposure to humans and other organisms. Presently, there is little understanding of the potential toxic effects of nanoparticle exposure. Nano-sized metal oxides, for example, may adversely affect biological systems due to their unique physiochemical properties. However, current findings are largely inconclusive and need further examination. The purpose of this study is to address the current knowledge gaps in metal oxide nanoparticle toxicity and to provide insight into the molecular mechanisms involved in exposure response. We evaluated the in vivo toxicity of CuO, ZnO, and TiO₂ nanoparticles to the soil nematode Caenorhabditis elegans (C. elegans). Metal oxide nanoparticle toxicity was assessed by using nematode mortality, fertility, and gene expression as endpoints. For toxicity assays, age-synchronized worms were exposed to nanoparticle treatments of various concentrations (range: 1-100 mg/L) and then evaluated for potential dose and/or time-dependent effects. The results of the lethality and fertility assays suggest that CuO and ZnO nanoparticles are more toxic than TiO₂ nanoparticles, causing increased nematode mortality as well as reduced offspring yields. Both CuO and ZnO nanoparticles were found to exhibit comparable toxicity to C. elegans within the tested dose range. In addition, ZnO nanoparticle-induced expression of select nematode genes was investigated using quantitative real-time PCR (qRT-PCR). Expression analysis revealed that gcs-1 was significantly up-regulated compared to the control after exposure to ZnO nanoparticles. As gcs-1 serves an important role in oxidative stress defense, functioning through the p38 mitogen-activated protein kinase (MAPK) pathway, these results might provide further insight into the molecular mechanisms involved in the response to metal oxide nanoparticle exposure.en_US
dc.description.degreeM.S.en_US
dc.format.extent89 p.en_US
dc.format.mediumdissertations, academicen_US
dc.identifier.urihttp://hdl.handle.net/10342/3826
dc.language.isoen_US
dc.publisherEast Carolina Universityen_US
dc.subjectBiologyen_US
dc.subjectC. elegans
dc.subject.lcshNanoparticles--Toxicology
dc.subject.lcshNanoparticles--Research
dc.subject.lcshToxicity testing--In vivo
dc.subject.lcshCaenorhabditis elegans
dc.subject.lcshCopper oxide--Toxicity testing
dc.subject.lcshZinc oxide--Toxicity testing
dc.subject.lcshTitanium dioxide--Toxicity testing
dc.titleTOXICITY OF METAL OXIDE NANOPARTICLES TO CAENORHABDITIS ELEGANSen_US
dc.typeMaster's Thesisen_US

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