Abstract
Low-intensity lasers are used for prevention and management of oral mucositis induced by anticancer therapy, but the effectiveness of treatment depends on the genetic characteristics of affected cells. This study evaluated the survival and induction of filamentation of Escherichia coli cells deficient in the nucleotide excision repair pathway, and the action of T4endonuclease V on plasmid DNA exposed to low-intensity red and near-infrared laser light. Cultures of wild-type (strain AB1157) E. coli and strain AB1886 (deficient in uvrA protein) were exposed to red (660 nm) and infrared (808 nm) lasers at various fluences, powers and emission modes to study bacterial survival and filamentation. Also, plasmid DNA was exposed to laser light to study DNA lesions produced in vitro by T4endonuclease V. Low-intensity lasers:i) had no effect on survival of wild-type E. coli but decreased the survival of uvrA protein-deficient cells,ii) induced bacterial filamentation, iii) did not alter the electrophoretic profile of plasmids in agarose gels, andiv) did not alter the electrophoretic profile of plasmids incubated with T4 endonuclease V. These results increase our understanding of the effects of laser light on cells with various genetic characteristics, such as xeroderma pigmentosum cells deficient in nucleotide excision pathway activity in patients with mucositis treated by low-intensity lasers.
Highlights
Oral mucositis is a common inflammatory process caused by chemotherapy and radiotherapy against head and neck cancers [1]
This study evaluated survival and filamentation induction in E. coli cells deficient in the nucleotide excision repair pathway, and the action of T4 endonuclease V on plasmid DNA exposed to low-intensity red and nearinfrared laser light
To ascertain whether the laser beam power had an effect on laser-induced biological effects, survival was determined in E. coli AB1157 and AB1886 cultures exposed to red and infrared lasers at increasing powers, with the highest fluence being 100 J/cm2 (Table 1)
Summary
Oral mucositis is a common inflammatory process caused by chemotherapy and radiotherapy against head and neck cancers [1]. Use of low-intensity lasers to treat mucositis has gained in importance, and has been successful in prevention and management of oral mucositis induced by anticancer therapy [4]. Because of their biostimulatory effect, red and nearinfrared lasers, which are nonthermal and nondestructive at low intensity, are widely used in a variety of health care settings for mucositis and other soft tissue repair. While the controversies about laser-induced DNA lesions by free radicals have not been resolved, it is interesting to evaluate whether other DNA repair pathways are involved in cellular responses to lowintensity lasers
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