Show simple item record

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.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. []en_US
dc.identifier.issn1090-2104 (Online)en_US
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.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

Files in this item


There are no files associated with this item.

This item appears in the following Collection(s)

Show simple item record