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dc.contributor.authorVan Dyk, E.en_US
dc.contributor.authorSteenkamp, A.en_US
dc.contributor.authorKoekemoer, G.en_US
dc.contributor.authorPretorius, P.J.en_US
dc.date.accessioned2012-02-29T09:45:50Z
dc.date.available2012-02-29T09:45:50Z
dc.date.issued2010en_US
dc.identifier.citationVan Dyk, E. et al. 2010. Hereditary tyrosinemia type 1 metabolites impair DNA excision repair pathways. Biochemical and biophysical research communications, 401(1):32-36. [https://doi.org/10.1016/j.bbrc.2010.09.002]en_US
dc.identifier.issn0006-291Xen_US
dc.identifier.issn1090-2104 (Online)en_US
dc.identifier.urihttp://hdl.handle.net/10394/5775
dc.identifier.urihttps://doi.org/10.1016/j.bbrc.2010.09.002
dc.identifier.urihttp://www.sciencedirect.com/science/article/pii/S0006291X10016773
dc.description.abstractHereditary tyrosinemia type 1 is an autosomal recessive metabolic disorder, which is caused by a defective fumarylacetoacetate hydrolase enzyme, and consequently metabolites such as succinylacetone and p-hydroxyphenylpyruvate accumulate. We used a modified comet assay to determine the effect of these metabolites on base- and nucleotide excision repair pathways. Our results indicate that the metabolites affected the repair mechanisms differently, since the metabolites had a bigger detrimental effect on BER than on NER
dc.publisherElsevieren_US
dc.subjectHereditary tyrosinemia
dc.subjectBase excision repair
dc.subjectNucleotide excision repair
dc.subjectComet assay
dc.titleHereditary tyrosinemia type 1 metabolites impair DNA excision repair pathwaysen_US
dc.contributor.researchID10176705 - Pretorius, Petrus Jacobus
dc.contributor.researchID10096353 - Koekemoer, Gerhard
dc.contributor.researchID12126497 - Van Dyk, Etresia


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