Cytotoxicity and mutagenesis induced by singlet oxygen in wild type and DNA repair deficient Escherichia coli strains

• Published in: DNA repair 2002-12, Vol.1 (12), p.1051-1056
• Main Authors: Cavalcante, Ana Karina Dias, Martinez, Glaucia Regina, Di Mascio, Paolo, Menck, Carlos Frederico Martins, Agnez-Lima, Lucymara Fassarella
• Format: Article
• Language: English
• Subjects: 8-Oxo-7,8-hydro-2′-deoxyguanosine; Biological and medical sciences; DNA Damage; DNA Glycosylases; DNA repair; DNA Repair - genetics; DNA, Bacterial - drug effects; DNA, Bacterial - genetics; DNA, Bacterial - metabolism; DNA-Formamidopyrimidine Glycosylase; Escherichia coli - drug effects; Escherichia coli - genetics; Escherichia coli - metabolism; Escherichia coli Proteins; FPG; Fundamental and applied biological sciences. Psychology; Molecular and cellular biology; Molecular genetics; Mutagenesis; Mutagenesis. Repair; MutY-glycosylase; N-Glycosyl Hydrolases - genetics; N-Glycosyl Hydrolases - metabolism; Singlet oxygen; Singlet Oxygen - toxicity
• ISSN: 1568-7864; 1568-7856
• DOI: 10.1016/S1568-7864(02)00164-7

Singlet oxygen ( 1 O 2 ) is a product of several biological processes and can be generated in photodynamic therapy, through a photosensitization type II mechanism. 1 O 2 is able to interact with lipids, proteins and DNA, leading to cell killing and mutagenesis, and can be directly involved with degenerative processes such as cancer and aging. In this work, we analyzed the cytotoxicity and mutagenesis induced after direct treatment of wild type and the DNA repair fpg and/or mutY deficient Escherichia coli strains with disodium 3,3′-(1,4-naphthylidene) diproprionate endoperoxide (NDPO 2), which releases 1 O 2 by thermodissociation. The treatment induced cell killing and mutagenesis in all strains, but the mutY strain showed to be more sensitive. These results indicate that even 1 O 2 generated outside bacterial cells may lead to DNA damage that could be repaired by pathways that employ MutY protein. As 1 O 2 is highly reactive, its interaction with cell membranes may generate secondary products that could react with DNA, leading to mutagenic lesions.