作者: Solveig Margrethe B. Lakså
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摘要: DNA lesions are introduced in all living organisms every day, both via endogenous processes and by exposure to an array of damaging agents. require repair for the sustenance life. Base excision (BER) nucleotide (NER) pathways involved removal oxidative helix-distorting lesions, respectively. Several studies suggest interactions or crosstalk between these pathways, involving overlapping activities same types but also interference pathways. Non-repaired regarded as important risk factor pathogenesis certain conditions diseases. It is gain insight interplay agents, their since this may be related overall sensitivity cells combined exogenous In present study, we aimed at studying exposures environmental genotoxicants low doses, potential The two lead that processed different We studied impact levels stress on lesions; vice versa - lesions. induced genetic background, study whether a lack could affect For purpose, utilised wild type mouse embryonic fibroblasts (Ogg1+/+ MEFs), MEF cell line deficient protein 8-oxoguanine glycosylase (Ogg1) (Ogg1-/- MEFs). Ogg1 gene oxidized BER. Ogg1+/+ MEFs exposed agent did not show perturbed suggesting NER-sensitive damage do influence Furthermore, (Ogg1+/+) Ogg1-/- was (single) level stress, reactive oxygen species (ROS) BER-sensitive However, showed more efficient compared MEFs, regardless DNA. This finding suggests BER-related play role conclusion, seem perturb cellular respectively, Ogg1-deficient MEFs. A however observed, BER NER with respect damage.