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Bacterial viability and oxidative stress
CO2 modulate oxidative stress
During these last four years we have developed a new axis of research dealing with CO2 impact on oxidative stress. This new axis was based on a recent paper from I. Fridovich lab’s indicating a link between Reactive oxygen species (ROS) and CO2 in vitro (Liochev and Fridovich, 2004). For this purpose we have designed and developed (in relation with Jacomex Company) a chamber allowing us to control the atmospheric CO2 level within it. Benjamin Ezraty (CR2) is in charge of this project since 2007 (in association with Maïalène Chabalier (tech.)) and he is responsible for major advances of this topic. ROS, which encompass the superoxide anion (O2•-), hydrogen peroxide (H2O2) and the hydroxyl radical (HO•), are harmful as they can oxidize all biological macromolecules (Finkel and Holbrook, 2000). in vitro metal-catalyzed reactions between CO2 and ROS can generate the harmful carbonate radical (CO3•-) (Liochev and Fridovich, 2004). In vivo, CO2 is both a major by-product of metabolism and the major pH buffer system in higher eukaryotes. CO2 is also required for the growth of many microorganisms (Walker, 1932). We thus tested whether atmospheric CO2 (current value 389 ppm) could exacerbate oxidative stress. We used E. coli as model organism to evaluate whether atmospheric CO2 influenced oxidative stress. We established that the minimal atmospheric CO2 concentration required for optimal growth was 40 ppm. We show that atmospheric CO2 (range studied : 40 to 1,000 ppm) increases the death of Escherichia coli caused by peroxide stress in a dose-specific fashion. This effect correlates with increases in H2O2-induced mutagenesis rates and DNA bases oxidation as measured by the amount of 8-oxo-guanine in the cell. Moreover, survival of mutants sensitive to aerobic growth (Hpx- dps and recA fur) (Park and Imlay, 2005 ; Touati et al., 1995), presumably due to their inability to tolerate oxygen-derived ROS, appear to be CO2 level-dependent (range studied : 40 to 1,000 ppm). The aerobic viability defect of these strains has been attributed to DNA damage caused by a Fenton reaction-based hydroxyl radical (HO•) production (Finkel and Holbrook, 2000 ; Park and Imlay, 2005 ; Touati et al., 1995). The higher oxygen toxicity at higher CO2 concentrations thus indicates that CO2 exacerbates HO•–induced DNA damage. Altogether these results indicate that atmospheric CO2 exacerbates ROS toxicity by increasing oxidative cellular lesions. This study provides the first evidence that oxidative stress is exacerbated by atmospheric CO2. CO2 have been a major point of focus, due to their contribution to the greenhouse effect (Cox et al., 2000), and increases in these levels are thought to be associated with global warming. In the light of the Special Report on Emissions Scenario, predicting that the atmosphere in 2100 will contain 1,000 ppm CO2 (Schneider, 2009) our results suggest that increases in atmospheric CO2 concentration have toxic effects over and above those of global warming Ezraty et al.,(2011)
