Acetaldehyde induces NER repairable mutagenic DNA lesions.

Autor:	Sonohara Y; Graduate School of Engineering Science, Osaka University, 1-3 Machikaneyama, Toyonaka, Osaka, Japan., Takatsuka R; Graduate School of Engineering Science, Osaka University, 1-3 Machikaneyama, Toyonaka, Osaka, Japan., Masutani C; Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya, Japan., Iwai S; Graduate School of Engineering Science, Osaka University, 1-3 Machikaneyama, Toyonaka, Osaka, Japan., Kuraoka I; Graduate School of Engineering Science, Osaka University, 1-3 Machikaneyama, Toyonaka, Osaka, Japan.; Department of Chemistry, Faculty of Science, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka, Japan.
Jazyk:	angličtina
Zdroj:	Carcinogenesis [Carcinogenesis] 2022 Feb 11; Vol. 43 (1), pp. 52-59.
DOI:	10.1093/carcin/bgab087
Abstrakt:	Nucleotide excision repair (NER) is a repair mechanism that removes DNA lesions induced by UV radiation, environmental mutagens and carcinogens. There exists sufficient evidence against acetaldehyde suggesting it to cause a variety of DNA lesions and be carcinogenic to humans. Previously, we found that acetaldehyde induces reversible intra-strand GG crosslinks in DNA similar to those induced by cis-diammineplatinum(II) that is subsequently repaired by NER. In this study, we analysed the repairability by NER mechanism and the mutagenesis of acetaldehyde. In an in vitro reaction setup with NER-proficient and NER-deficient xeroderma pigmentosum group A (XPA) cell extracts, NER reactions were observed in the presence of XPA recombinant proteins in acetaldehyde-treated plasmids. Using an in vivo assay with living XPA cells and XPA-correcting XPA cells, the repair reactions were also observed. Additionally, it was observed that DNA polymerase eta inserted dATP opposite guanine in acetaldehyde-treated oligonucleotides, suggesting that acetaldehyde-induced GG-to-TT transversions. These findings show that acetaldehyde induces NER repairable mutagenic DNA lesions. (© The Author(s) 2021. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)
Databáze:	MEDLINE
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