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dc.contributor.advisorHampton, Mark
dc.contributor.advisorBetz, Andrea
dc.contributor.advisorO'Connor, Karina
dc.contributor.authorVick, Kate Angela
dc.date.available2013-11-11T01:14:05Z
dc.date.copyright2013
dc.identifier.citationVick, K. A. (2013). Functional consequences of lowering mitochondrial peroxiredoxin 3 expression (Thesis, Bachelor of Biomedical Sciences with Honours). University of Otago. Retrieved from http://hdl.handle.net/10523/4412en
dc.identifier.urihttp://hdl.handle.net/10523/4412
dc.description.abstractPeroxiredoxin 3 (Prx 3) is an abundant mitochondrial protein that is very effective at scavenging hydroperoxides. The overexpression of Prx 3 has been shown to protect cells from oxidative stress and apoptosis, and knockout studies show an increase in intracellular ROS levels and oxidative stress. However, the knockout phenotype is mild and there has been no in-depth characterization of the effects of Prx 3 knockdown on mitochondrial function in response to oxidative stress. In this study, Prx 3 expression was knocked down to approximately 10-20% in a HeLa cell line, over a 5-6 day period. An inducible small hairpin RNA (shRNA) system was used to achieve this and no significant compensatory increase by other members of the Prx family was observed. These cells showed no difference in cell viability in response to exogenous H2O2, or during increased mitochondrial H2O2 production by the respiratory chain inhibitors; rotenone and antimycin A. Mitochondrial respiration was measured in intact cells with a Seahorse Extracellular Flux Analyzer and while the Prx 3 knockdown cells appeared to have normal rates of O2 consumption under basal conditions, mitochondrial stress was more detrimental in these cells. Overall, Prx 3 knockdown had a relatively limited phenotype, suggesting that low levels of Prx 3 are sufficient to protect cells from oxidative stress, or that Prx 3 may have a more important role as a sensor and signalling molecule than as a direct antioxidant protein.
dc.language.isoen
dc.publisherUniversity of Otago
dc.rightsAll items in OUR Archive are provided for private study and research purposes and are protected by copyright with all rights reserved unless otherwise indicated.
dc.subjectPeroxiredoxin
dc.subjectPeroxiredoxin3
dc.subjectknockdown
dc.titleFunctional consequences of lowering mitochondrial peroxiredoxin 3 expression
dc.typeThesis
dc.date.updated2013-11-11T00:51:12Z
dc.language.rfc3066en
thesis.degree.disciplinePathology
thesis.degree.nameBachelor of Biomedical Sciences with Honours
thesis.degree.grantorUniversity of Otago
thesis.degree.levelHonours
otago.interloanno
otago.openaccessAbstract Only
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