| dc.contributor.author | Van Dyk, E. | en_US |
| dc.contributor.author | Steenkamp, A. | en_US |
| dc.contributor.author | Koekemoer, G. | en_US |
| dc.contributor.author | Pretorius, P.J. | en_US |
| dc.date.accessioned | 2012-02-29T09:45:50Z | |
| dc.date.available | 2012-02-29T09:45:50Z | |
| dc.date.issued | 2010 | en_US |
| dc.identifier.citation | Van 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.issn | 0006-291X | en_US |
| dc.identifier.issn | 1090-2104 (Online) | en_US |
| dc.identifier.uri | http://hdl.handle.net/10394/5775 | |
| dc.identifier.uri | https://doi.org/10.1016/j.bbrc.2010.09.002 | |
| dc.identifier.uri | https://www.sciencedirect.com/science/article/pii/S0006291X10016773 | |
| dc.description.abstract | Hereditary 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.publisher | Elsevier | en_US |
| dc.subject | Hereditary tyrosinemia | |
| dc.subject | Base excision repair | |
| dc.subject | Nucleotide excision repair | |
| dc.subject | Comet assay | |
| dc.title | Hereditary tyrosinemia type 1 metabolites impair DNA excision repair pathways | en_US |
| dc.contributor.researchID | 10176705 - Pretorius, Petrus Jacobus | |
| dc.contributor.researchID | 10096353 - Koekemoer, Gerhard | |
| dc.contributor.researchID | 12126497 - Van Dyk, Etresia | |
