We can thus propose that antioxidative defense systems of D. vulgaris Hildenborough can overcome the negative effects of low-peroxide stress, and so after an initial increase in the transcriptional responses, the gene expression levels revert to basic levels after elimination of H2O2.

Because high-peroxide stresses are too deleterious for the cells, the corresponding genes (most of them encoding Fe-containing proteins) are downregulated to limit free-metal-induced damages and increase survival. Rubrerythrins encoding genes (rbr1 and rbr2) were the most upregulated members of the PerR regulon at the transcript level under low-peroxide stress (0.1 mM H2O2, 30 min). Previously, they have been identified as important enzymes for oxygen ICG-001 clinical trial http://www.selleckchem.com/products/dabrafenib-gsk2118436.html and other oxidative stresses (Fournier et al., 2003). Interestingly, the sor gene was also strongly upregulated under such peroxide

stress conditions, whereas no significant upregulation of this candidate was observed during 0.1% O2 exposure (Mukhopadhyay et al., 2007). Therefore, NADH-dependent H2O2 peroxidases (rubrerythrins, nigerythrin), together with thiol peroxidase and SOR, might play a major role in the H2O2 stress response. Transcript analysis revealed that gene expression reverted to the same level as in untreated cells and even lower for a time period longer than 30 min (0.1 mM H2O2 stress), which can explain the continuing decrease in peroxidase-specific activity during the 60–240 min of exposure. H2O2 quantification revealed that H2O2 was rapidly consumed over time and no remaining H2O2 could be detected after 90 min when either 0.1 or 0.3 mM was added. It should

be noted that oxidized compounds (for instance, polysulfide) could be formed due to the chemical reaction between H2O2 and hydrogen sulfide produced by D. vulgaris cells. It should be also noted that the presence of H2S is the physiologic situation for these cells in their biotopes, and the addition of H2O2 (as ROS formed under temporary oxic conditions) to H2S-producing cells can be considered as quite normal. Even if PDK4 we cannot exclude that a part of H2O2 was chemically reduced by the end-product of the sulfate reduction, our data suggest that the observed H2O2 consumption corresponds to a cell-mediated reaction. Most probably, H2O2 stresses include direct effects from H2O2 itself and indirect effects from H2O2-derived reactive chemical species together with increased redox potential. The data show that addition of either 0.1 or 0.3 mM H2O2 to a mid-exponential culture results in a rapid consumption of the H2O2 in a cell-mediated reaction. However, exposure to 0.3 mM H2O2 appears to be much more toxic to the cells as all tested genes were strongly downregulated even when H2O2 was no longer detectable in the culture. This phenomenon provides evidence for the high stress state of the cells, which is not the case when they are exposed to a lower concentration of H2O2 (0.1 mM). In the presence of 0.