Acidification of East Siberian Arctic Shelf waters through addition of freshwater and terrestrial carbon

Ocean acidification affects marine ecosystems and carbon cycling, and is considered a direct effect of anthropogenic carbon dioxide uptake from the atmosphere1–3 . Accumulation of atmospheric CO2 in ocean surface waters is predicted to make the ocean twice as acidic by the end of this century4 . The ArcticOcean is particularly sensitive to ocean acidification becausemoreCO2 candissolveincoldwater5,6 .Herewepresent observations of the chemical and physical characteristics of EastSiberianArctic Shelfwatersfrom1999,2000–2005,2008 and 2011, and find extreme aragonite undersaturation that reflects acidity levels in excess of those projected in this region for 2100. Dissolved inorganic carbon isotopic data and Markov chain Monte Carlo simulations of water sources using salinity andδ18 Odata suggest that the persistent acidification is driven by the degradation of terrestrial organic matter and discharge of Arctic river water with elevated CO2 concentrations, rather than by uptake of atmospheric CO2 . We suggest that East Siberian Arctic Shelf waters may become more acidic if thawing permafrost leads to enhanced terrestrial organic carbon inputs and if freshwater additions continue to increase, which may affect their efficiency as a source of CO2

Mitochondrial metabolism and cancer

International audienceGlycolysis has long been considered as the major metabolic process for energy production and anabolic growth in cancer cells. Although such a view has been instrumental for the development of powerful imaging tools that are still used in the clinics, it is now clear that mitochondria play a key role in oncogenesis. Besides exerting central bioen-ergetic functions, mitochondria provide indeed building blocks for tumor anabolism, control redox and calcium ho-meostasis, participate in transcriptional regulation, and govern cell death. Thus, mitochondria constitute promising targets for the development of novel anticancer agents. However, tumors arise, progress, and respond to therapy in the context of an intimate crosstalk with the host immune system, and many immunological functions rely on intact mitochondrial metabolism. Here, we review the cancer cell-intrinsic and cell-extrinsic mechanisms through which mitochondria influence all steps of oncogenesis, with a focus on the therapeutic potential of targeting mitochondrial metabolism for cancer therapy