A team from the Bacterial Chemistry Laboratory (CNRS, Marseilles) has just shown that carbon dioxide (CO2) is involved in oxidative damage in vivo. Indeed, in the model organism Escherichia coli, certain types of damage due to oxidative stress (cell death, DNA lesions, mutation frequency etc.) are aggravated at higher atmospheric concentrations of CO2. The range of CO2 concentrations studied extended from 40 ppm to the values predicted for 2100 (1000 ppm). These results indicate that the predicted increase in atmospheric CO2 concentration should have a direct effect on living organisms. This work will be published in EMBO Reports on February 25th 2011.
Air pollution, cigarette smoke, chemicals, food additives, physical stress and the normal use of oxygen by our bodies contribute to the production of compounds (so-called “reactive oxygen species” or ROS) that cause various degrees of oxidative damage to cells: genetic mutations, carcinogenesis, protein oxidation.
The “Bacterial Viability and Oxidative Stress” team directed by Sam Dukan at the Laboratoire de Chimie Bactérienne (a CNRS laboratory at the Institute of Mediterranean Microbiology, a structure affiliated to both the CNRS and the University of the Mediterranean) investigates the role of various ROS in the process of cell death. The most recent work of this team, on the model bacterium Escherichia coli, reveals the important role of a new actor in oxidative damage in vivo: carbon dioxide (CO2).
The researchers asked Jacomex to develop a prototype “glove box” apparatus in which it was possible to control CO2 concentrations whilst maintaining oxygen concentration at a fixed level (20%, as in the atmosphere). With the help of this tool, making it possible to reproduce the atmospheres of yesterday, today and tomorrow (in terms of oxygen, nitrogen and carbon dioxide concentrations), they evaluated the effects on E. coli of an oxidative stress (hydrogen peroxide, H2O2), at various atmospheric CO2 concentrations (40 to 1000 ppm; current concentration: 389 ppm). They found that increases in CO2 concentration were associated with increases in cell death, DNA mutation rate and the number of DNA lesions in response to oxidative stress.
The authors of this study suggest that this phenomenon may be due to the occurrence of reactions in vivo between CO2 and the various ROS, leading to the formation of free radicals, such as the carbonate radical (CO3•-). Indeed, this reaction has already been demonstrated in vitro, and this radical has broad target specificity. For example, its reaction with DNA seems to involve principally guanine, a target that the researchers found to be affected by CO2 concentration. This team has also shown that the physiological characteristics of E. coli (intracellular pH, metabolic pathways, defence against ROS, protein turnover rates etc.) are not affected by CO2 concentration, thus excluding all other possible interpretations of the damage observed.
Given the range of CO2 concentrations studied, this work suggests that the predicted increase in atmospheric CO2 concentration (to 1000 ppm in 2100) could have direct effects on living organisms, such as bacteria (increase in the frequencies of certain DNA lesions and of mutation).
Sam Dukan team’s is continuing its work on E. coli, with the characterisation of various mutations. The researchers also wish to study the possible role of carbonic anhydrase in the oxidative stress response. They would like to carry out collaborative studies with other research teams on more highly evolved organisms, such as mice. The objective: to study the link between atmospheric CO2 concentration and the occurrence of diseases that are known to be associated with oxidative stress (e.g. neurodegenerative diseases, cancers).
CO2 exacerbates oxygen toxicity. Benjamin Ezraty, Maïalène Chabalier, Adrien Ducret, Etienne Maisonneuve and Sam Dukan Aix Marseille Université – Laboratoire de Chimie Bactérienne (UPR 9043) – Institut de Microbiologie de la Méditerranée (IFR88) – CNRS, 31, Chemin Joseph Aiguier, 13402, Marseille, France. EMBO reports, 25th February 2011.
CNRS researcher l Sam Dukan l T 00 33 (0)6 61 93 49 29 l firstname.lastname@example.org