An assessment of the carbon balance of Arctic tundra:Comparisons among observations, process models, and atmospheric inversions

Although Arctic tundra has been estimated to cover only 8% of the global land surface, the large and potentially labile carbon pools currently stored in tundra soils have the potential for large emissions of carbon (C) under a warming climate. These emissions as radiatively active greenhouse gases in the form of both CO<sub>2</sub> and CH<sub>4</sub> could amplify global warming. Given the potential sensitivity of these ecosystems to climate change and the expectation that the Arctic will experience appreciable warming over the next century, it is important to assess whether responses of C exchange in tundra regions are likely to enhance or mitigate warming. In this study we compared analyses of C exchange of Arctic tundra between 1990 and 2006 among observations, regional and global applications of process-based terrestrial biosphere models, and atmospheric inversion models. Syntheses of flux observations and inversion models indicate that the annual exchange of CO<sub>2</sub> between Arctic tundra and the atmosphere has large uncertainties that cannot be distinguished from neutral balance. The mean estimate from an ensemble of process-based model simulations suggests that Arctic tundra has acted as a sink for atmospheric CO<sub>2</sub> in recent decades, but based on the uncertainty estimates it cannot be determined with confidence whether these ecosystems represent a weak or a strong sink. Tundra was 0.6 °C warmer in the 2000s compared to the 1990s. The central estimates of the observations, process-based models, and inversion models each identify stronger sinks in the 2000s compared with the 1990s. Some of the process models indicate that this occurred because net primary production increased more in response to warming than heterotrophic respiration. Similarly, the observations and the applications of regional process-based models suggest that CH<sub>4</sub> emissions from Arctic tundra have increased from the 1990s to 2000s because of the sensitivity of CH<sub>4</sub> emissions to warmer temperatures. Based on our analyses of the estimates from observations, process-based models, and inversion models, we estimate that Arctic tundra was a sink for atmospheric CO<sub>2</sub> of 110 Tg C yr<sup>−1</sup> (uncertainty between a sink of 291 Tg C yr<sup>−1</sup> and a source of 80 Tg C yr<sup>−1</sup>) and a source of CH<sub>4</sub> to the atmosphere of 19 Tg C yr<sup>−1</sup> (uncertainty between sources of 8 and 29 Tg C yr<sup>−1</sup>). The suite of analyses conducted in this study indicate that it is important to reduce uncertainties in the observations, process-based models, and inversions in order to better understand the degree to which Arctic tundra is influencing atmospheric CO<sub>2</sub> and CH<sub>4</sub> concentrations. The reduction of uncertainties can be accomplished through (1) the strategic placement of more CO<sub>2</sub> and CH<sub>4</sub> monitoring stations to reduce uncertainties in inversions, (2) improved observation networks of ground-based measurements of CO<sub>2</sub> and CH<sub>4</sub> exchange to understand exchange in response to disturbance and across gradients of climatic and hydrological variability, and (3) the effective transfer of information from enhanced observation networks into process-based models to improve the simulation of CO<sub>2</sub> and CH<sub>4</sub> exchange from Arctic tundra to the atmosphere

Organotin plant uptake from a contaminated soil: phytoaccumulation and biotransformation into cultivated plant

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Mitochondrial complex I inhibition triggers a mitophagy-dependent ROS increase leading to necroptosis and ferroptosis in melanoma cells

Contains fulltext : 174431.pdf (publisher's version ) (Open Access)Inhibition of complex I (CI) of the mitochondrial respiratory chain by BAY 87-2243 ('BAY') triggers death of BRAFV600E melanoma cell lines and inhibits in vivo tumor growth. Here we studied the mechanism by which this inhibition induces melanoma cell death. BAY treatment depolarized the mitochondrial membrane potential (Deltapsi), increased cellular ROS levels, stimulated lipid peroxidation and reduced glutathione levels. These effects were paralleled by increased opening of the mitochondrial permeability transition pore (mPTP) and stimulation of autophagosome formation and mitophagy. BAY-induced cell death was not due to glucose shortage and inhibited by the antioxidant alpha-tocopherol and the mPTP inhibitor cyclosporin A. Tumor necrosis factor receptor-associated protein 1 (TRAP1) overexpression in BAY-treated cells lowered ROS levels and inhibited mPTP opening and cell death, whereas the latter was potentiated by TRAP1 knockdown. Knockdown of autophagy-related 5 (ATG5) inhibited the BAY-stimulated autophagosome formation, cellular ROS increase and cell death. Knockdown of phosphatase and tensin homolog-induced putative kinase 1 (PINK1) inhibited the BAY-induced Deltapsi depolarization, mitophagy stimulation, ROS increase and cell death. Dynamin-related protein 1 (Drp1) knockdown induced mitochondrial filamentation and inhibited BAY-induced cell death. The latter was insensitive to the pancaspase inhibitor z-VAD-FMK, but reduced by necroptosis inhibitors (necrostatin-1, necrostatin-1s)) and knockdown of key necroptosis proteins (receptor-interacting serine/threonine-protein kinase 1 (RIPK1) and mixed lineage kinase domain-like (MLKL)). BAY-induced cell death was also reduced by the ferroptosis inhibitor ferrostatin-1 and overexpression of the ferroptosis-inhibiting protein glutathione peroxidase 4 (GPX4). This overexpression also inhibited the BAY-induced ROS increase and lipid peroxidation. Conversely, GPX4 knockdown potentiated BAY-induced cell death. We propose a chain of events in which: (i) CI inhibition induces mPTP opening and Deltapsi depolarization, that (ii) stimulate autophagosome formation, mitophagy and an associated ROS increase, leading to (iii) activation of combined necroptotic/ferroptotic cell death

Evaluation of a combined fractionation and speciation approach for study of size-based distribution of organotin species on environmental colloids

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