Lipid peroxidation product 4-hydroxy-2-nonenal modulates base excision repair in human cells

Article ID	Journal	Published Year	Pages	File Type
8320766	DNA Repair	2014	11 Pages	PDF

Abstract

- BER is deregulated by the major lipid peroxidation product 4-hydroxynonenal (HNE).
- Excision of ethenobases and ligation is inhibited, while AP-site incision is stimulated.
- Such imbalance increases the number of SSBs in cells exposed to MMS or H2O2.
- This may be an additional mechanism of genotoxic effects of inflammation.

Keywords

APE1 MMS HNE PNK ACR BER MSI FPG 8-oxoG LPO CRO OGG1 TCr CSB GST MDA ANPG PBS ɛC ɛA X-Ray Repair Cross-Complementing Protein 1 THF MBD4 XRCC1 CAA TDG IPTG DTT AP-site 4-hydroxy-2-nonenal 4-Hydroxy-2-hexenal 8-oxoguanine glycosylase 1 8-oxoguanine apurinic/apyrimidinic site BSA Thymine DNA glycosylase DNA single strand breaks hTERT SSBs bovine serum albumin Acrolein EDTA Ethylenediaminetetraacetic acid Polyunsaturated fatty acids PUFA isopropyl β-D-1-thiogalactopyranoside Microsatellite instability trans-4-Hydroxy-2-nonenal Transcription-coupled repair base excision repair human telomerase reverse transcriptase Par Hhe dithiothreitol Colorectal cancer Phosphate buffered saline malondialdehyde methyl methanesulfonate Lipid peroxidation Poly(ADP-ribose)polynucleotide kinase CRC glutathione S-transferase