Title: Incomplete base excision repair contributes to cell death from antibiotics and other stresses.
Authors: Gruber, Charley C; Walker, Graham C
Published In DNA Repair (Amst), (2018 11)
Abstract: Numerous lethal stresses in bacteria including antibiotics, thymineless death, and MalE-LacZ expression trigger an increase in the production of reactive oxygen species. This results in the oxidation of the nucleotide pool by radicals produced by Fenton chemistry. Following the incorporation of these oxidized nucleotides into the genome, the cell's unsuccessful attempt to repair these lesions through base excision repair (BER) contributes causally to the lethality of these stresses. We review the evidence for this phenomenon of incomplete BER-mediated cell death and discuss how better understanding this pathway could contribute to the development of new antibiotics.
PubMed ID: 30181041
MeSH Terms: Animals; Anti-Bacterial Agents/pharmacology*; Anti-Bacterial Agents/toxicity; Cell Death/drug effects*; DNA Damage*; DNA Repair*; DNA/metabolism; Eukaryota/drug effects; Eukaryota/genetics; Eukaryota/metabolism; Humans; Oxidative Stress; Reactive Oxygen Species/metabolism*