Namic inactivation (PDI) of S. aureus is also a promising option. Photodynamic inactivation is based on a concept that a non toxic chemical, named a photosensitizer upon excitation with light of an appropriate wavelength is activated. As a consequence singlet oxygen and other reactive oxygen species are produced, which are responsible for thecytotoxic effect towards bacterial cells [37,38]. It is of great clinical importance and an advantage of PDI that S. aureus isolates, both MRSA and MSSA, can be effectively killed [39]. Previous reports of our group emphasized that S. aureus response to PDI is a straindependant phenomenon, which from the clinical point of view warrants attention [24]. Among 80 MRSA and MSSA strains some were ultra-sensitive to protoporphyrin IX diarginate-based PDI, whereas others exerted complete resistance to such treatment. The same tendency was observed in the presented results with the use of protoporphyrin IX as a photosensitizer (Figure 3). In our attempts to determine the molecular marker of strain-dependent response to PDI, we found that biofilm producing strains were killed less efficiently in comparison to non biofilm-producing strains [24], whereas efflux pumps, eg. NorA had no influence on the efficacy of photokilling [25].Sod status and PDI responseIn the presented work we focused on the role of superoxide dismutases in the response of S. aureus to PDI. Superoxide dismutase constitutes the first line of bacterial defense against order SB 202190 oxidative stress, therefore it was expected that the correlation may exist between the Sod status in the cell and response to PDI. Statistical analysis revealed no substantial difference in the survival rate among the four reference strains in TSB medium. In the study by Valderas and Hart, the same strains, deprived of either of the two Sods or both of them, were analyzed in conditions of methyl viologen (MV)-generated oxidative stress. They noticed that the highest drop in viability was observed in the case of SodAM double mutants grown in TSB medium [8]. On the contrary, the group of Foster, found that similar strains (i.e. analogues Sod mutants but with different genetic background) due toNakonieczna et al. BMC Microbiology 2010, 10:323 http://www.biomedcentral.com/1471-2180/10/Page 9 ofthe action of internally-generated superoxide anion, viability drops in the case of both, SodA and SodAM double mutants in the Chelex treated BHI medium without Mn++ ions. They also observed that upon supplementation of the medium with Mn++ the viability of the mentioned mutants increased. When the same strains were challenged with externally generated superoxide anion in the stationary phase of growth, only the double Sod mutant was more susceptible to such treatment in comparison to the wild type SH1000 strain, moreover such an effect was not dependent on Mn++ presence [16]. We performed statistical analysis of the data presented in Figure 1 and found no statistically relevant difference existing among the four strains analyzed (i.e. wild type RN6390, RN6390sodA::tet, RN6390sodM::erm, RN6390sodM::erm sodA::tet), what is seen PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28212752 in Figure 1. Our results differ from the one presented by Hart [8], which may be attributed to the differences in types of oxidative stress generated as a result of photodynamic action versus methyl viologen-induced oxidative stress used by Hart group. Methyl viologen is believed to induce internal oxidative stress. Our previous results showed that PDI-induced oxidative.