Book Description

The 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.