Articles by Eugene A. Gibbs-Flournoy in JoVE
Abordagens para avaliação de estresse oxidativo toxicológico usando sensores Fluorogenic geneticamente codificado de imagem Elizabeth M. Corteselli1, James M. Samet2, Eugene A. Gibbs-Flournoy2,3 1Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, 2Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, 3Oak Ridge Institute for Science and Education Este manuscrito descreve o uso de repórteres fluorogenic geneticamente codificado em um aplicativo de imagem latente da viver-pilha para o exame de estresse oxidativo induzido por xenobiótico. Esta abordagem experimental oferece inigualável resolução spatiotemporal, sensibilidade e especificidade, evitando muitas das deficiências dos métodos convencionais utilizados para a detecção de estresse oxidativo toxicológico.
Other articles by Eugene A. Gibbs-Flournoy on PubMed
Darkfield-confocal Microscopy Detection of Nanoscale Particle Internalization by Human Lung Cells Particle and Fibre Toxicology. | Pubmed ID: 21247485 Concerns over the health effects of nanomaterials in the environment have created a need for microscopy methods capable of examining the biological interactions of nanoparticles (NP). Unfortunately, NP are beyond the diffraction limit of resolution for conventional light microscopy (~200 nm). Fluorescence and electron microscopy techniques commonly used to examine NP interactions with biological substrates have drawbacks that limit their usefulness in toxicological investigation of NP. EM is labor intensive and slow, while fluorescence carries the risk of photobleaching the sample and has size resolution limits. In addition, many relevant particles lack intrinsic fluorescence and therefore can not be detected in this manner. To surmount these limitations, we evaluated the potential of a novel combination of darkfield and confocal laser scanning microscopy (DF-CLSM) for the efficient 3D detection of NP in human lung cells. The DF-CLSM approach utilizes the contrast enhancements of darkfield microscopy to detect objects below the diffraction limit of 200 nm based on their light scattering properties and interfaces it with the power of confocal microscopy to resolve objects in the z-plane.
Neonatal Rat Age, Sex and Strain Modify Acute Antioxidant Response to Ozone Inhalation Toxicology. | Pubmed ID: 28880688 Chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the US and its impact continues to increase in women. Oxidant insults during critical periods of early life appear to increase risk of COPD through-out the life course. To better understand susceptibility to early life exposure to oxidant air pollutants we used Fisher (F344), Sprague-Dawley (SD) and Wistar (WIS) male and female neonatal rat pups to assess: (A) if strain (i.e. genetics), sex, or stage of early life development affected baseline lung antioxidant or redox enzyme levels and (B) if these same factors modulated antioxidant responsiveness to acute ozone exposure (1 ppm × 2 h) on post-natal day (PND) 14, 21, or 28. In air-exposed pups from PND14-28, some parameters were unchanged (e.g. uric acid), some decreased (e.g. superoxide dismutase), while others increased (e.g. glutathione recycling enzymes) especially post-weaning. Lung total glutathione levels decreased in F344 and SD pups, but were relatively unchanged in WIS pups. Post-ozone exposure, data suggest that: (1) the youngest (PND14) pups were the most adversely affected; (2) neonatal SD and WIS pups, especially females, were more prone to ozone effects than males of the same age and (3) F344 neonates (females and males) were less susceptible to oxidative lung insult, not unlike F344 adults. Differences in antioxidant levels and responsiveness between sexes and strains and at different periods of development may provide a basis for assessing later life health outcomes - with implications for humans with analogous genetic or dietary-based lung antioxidant deficits.