Spatial trends and historical deposition of mercury in eastern and northern Canada inferred from lake sediment cores.

Recent and historical deposition of mercury (Hg) was examined over a broad geographic area from southwestern Northwest Territories to Labrador and from the U.S. Northeast to northern Ellesmere Island using dated sediment cores from 50 lakes (18 in midlatitudes (41-50 degrees N), 14 subarctic (51-64 degrees N) and 18 in the Arctic (65-83 degrees N)). Distinct increases of Hg overtime were observed in 76% of Arctic, 86% of subarctic and 100% of midlatitude cores. Subsurface maxima in Hg depositional fluxes (microg m(-2) y(-1)) were observed in only 28% of midlatitude lakes and 18% of arctic lakes, indicating little recent reduction of inputs. Anthropogenic Hg fluxes adjusted for sediment focusing and changes in sedimentation rates (deltaF(adj,F)) ranged from -22.9 to 61 microg m(-2) y(-1) and were negatively correlated (r = -0.57, P < 0.001) with latitude. Hg flux ratios (FRs; post-1990)/pre-1850) ranged from 0.5 to 7.7. The latitudinal trend for Hg deltaF(adj,F) values showed excellent agreement with predictions of the global mercury model, GRAHM for the geographic location of each lake (r = 0.933, P < 0.001). The results are consistent with a scenario of slow atmospheric oxidation of mercury, and slow deposition of reactive mercury emissions, declining with increasing latitude away from emission sources in the midlatitudes, and support the view that there are significant anthropogenic Hg inputs in the Arctic.

IR spectroscopy applied subsequent to a proton transfer reaction in the excited state of isolated 3-hydroxyflavone and 2-(2-naphthyl)-3-hydroxychromone.

IR/R2PI-spectroscopy has been applied to the electronic ground and electronically excited states of 3-hydroxyflavone (3-HF) and 2-(2-naphthyl)-3-hydroxychromone (2-NHC) in a supersonic jet yielding direct structural information on the educt and product of a proton transfer reaction. We show that IR spectra of the electronically excited states can be recorded subsequent to a photoinduced chemical reaction, in this case a proton transfer. In combination with DFT and TDDFT calculations structural assignments are performed.

A subpopulation of mitochondria prevents cytosolic calcium overload in endothelial cells after cold ischemia/reperfusion.

BACKGROUND: Calcium represents a key mediator of cold ischemia/reperfusion (CIR) injury presumably by affecting mitochondrial function. In this study, we investigated cellular and mitochondrial changes of calcium homeostasis in sublethally damaged human endothelial cells. METHODS: Changes in cellular and mitochondrial calcium concentrations were studied after cold ischemia in University of Wisconsin solution for 12 hr and reperfusion in ringer solution. Cytosolic-free calcium concentration ([Ca2+]c) and mitochondrial-free calcium content ([Ca2+]m) were analyzed by fura-2 and rhod-2 fluorescence, respectively. Pretreatment of cells with ruthenium red (RR) or a H+-ionophore was used to inhibit mitochondrial calcium uptake. Mitochondrial membrane potential (DeltaPsim) was measured by 5,5',6,6'-tetrachloro- 1,1',3,3'-tetraethylbenzimidazolylcarbocyanine iodide and 3,3'-dihexyloxacarbocyanine iodide fluorescence. RESULTS: Twelve-hr cold ischemia did not induce apoptosis in endothelial cells. In such sublethally damaged cells, [Ca2+]c rose from approximately 20 nmol/L after cold ischemia to approximately 120 nmol/L during reperfusion. Pretreatment with RR leads to an approximately 5-fold rise in [Ca2+]c. Image analysis revealed a significant increase of [Ca2+]m in a subpopulation of mitochondria during reperfusion. This was not the case in RR-pretreated cells. DeltaPsim decreased significantly during cold ischemia and was sustained during reperfusion. The loss of DeltaPsim can be related to a reduced portion of mitochondria exhibiting high DeltaPsim. CONCLUSIONS: Our results suggest that cytosolic calcium influx during CIR is buffered by a selective portion of mitochondria in human umbilical vein endothelial cells. These mitochondria protect cells against cytosolic calcium overload and probably against subsequent cell injury.

Origin of cadmium and lead in clear softwater lakes of high-altitude and high-latitude, and their bioavailability and toxicity to fish.

As a consequence of atmospheric deposition, effects of pollutants such as acidification and metal contamination are evident even in remote aquatic ecosystems of mountain and polar regions. Due to similar environmental characteristics (e.g., oligotrophy, low buffering capacity, long ice-cover, high precipitation rates), clearwater high altitude and high latitude lakes represent very sensitive ecosystems, which are extremely susceptible to even slight changes of the environment. Thus, the environmental relevance of Cd and Pb for both types of lakes is discussed in relation to their extraordinary sensitivity to environmental changes. The impact of Cd and Pb on fish from high altitude and high latitude lakes is reviewed and biotic and abiotic factors controlling bioavailability and toxicity of metals to fish are summarized. Apart from direct toxic effects of low pH, acidification increases the bioavailability of metals for fish. Furthermore, low concentrations of dissolved organic carbon and suspended particles take influence on the uptake and toxicity of metals in fish from clear high altitude and high latitude lakes. Since even very low concentrations of Cd and Pb may result in high metal concentrations in fish, evaluation of critical metal loads for clear high altitude and high latitude lakes is of major importance.

The effect of ascorbate on proteolytic enzyme activities in fish.

In vitro studies showed that an ascorbic acid concentration of 15 mM depressed the trypsin activity in three fish species by 50%, whereas dehydroascorbic acid and ascorbic sulfate did not inhibit trypsin or chymotrypsin activities. However, this inhibitory action is unlikely in vivo because ascorbic acid is rapidly oxidized in the digestive tract content to the dehydroascorbic acid.