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Coastal wetlands, including freshwater systems near large lakes, rapidly bury carbon, but less is known about how they transport carbon either to marine and lake environments or to the atmosphere as greenhouse gases (GHGs) such as carbon dioxide and methane. This study examines how GHG production and organic matter (OM) mobility in coastal wetland soils vary with the availability of oxygen and other terminal electron acceptors. We also evaluated how OM and redox-sensitive species varied across different size fractions: particulates (0.45–1μm), fine colloids (0.1–0.45μm), and nano particulates plus truly soluble (<0.1μm; NP+S) during 21-day aerobic and anaerobic slurry incubations. Soils were collected from the center of a freshwater coastal wetland (FW-C) in Lake Erie, the upland-wetland edge of the same wetland (FW-E), and the center of a saline coastal wetland (SW-C) in the Pacific Northwest, USA. Anaerobic methane production for FW-E soils were 47 and 27,537 times greater than FW-C and SW-C soils, respectively. High Fe 2+ and dissolved sulfate concentrations in FW-C and SW-C soils suggest that iron and/or sulfate reduction inhibited methanogenesis. Aerobic CO 2 production was highest for both freshwater soils, which had a higher proportion of OM in the NP+S fraction (64±28% and 70±10% for FW-C and FW-E, respectively) and organic C:N ratios reflective of microbial detritus (5.3±5.3 and 5.3±7.0 for FW-E and FW-C, respectively) compared to SW-C, which had a higher fraction of particulate (58±9%) and fine colloidal (19±7%) OM and organic C:N ratios reflective of vegetation detritus (11.4 ± 1.7). The variability in GHG production and shifts in OM size fractionation and composition observed across freshwater and saline soils collected within individual and across different sites reinforce the high spatial variability in the processes controlling OM stability, mobility, and bioavailability in coastal wetland soils.

The fate of chromium (Cr) – a redox sensitive metal – in surface sediments is closely linked to early diagenetic processes. This review summarizes the main redox pathways that have been clearly identified over recent decades concerning the behavior of Cr(III,VI) in aquatic environments, and applies them to surface sediments where data for redox speciation remain limited. Overall, abiotic redox reactions that govern the speciation of Cr involve manganese (Mn) (III,IV) (hydr)-oxydes for Cr(III) oxidation, Cr(VI)-reducing species (dissolved iron (Fe) (II) and hydrosulfide (HS)−), and Cr(VI)-reducing phases (ferrous and sulfide minerals, as well as Fe(II)-bearing minerals). Bacterial activity is also responsible for the redox interconversion between Cr(III) and Cr(VI): biotic reduction of Cr(VI) to Cr(III) is observed through either detoxification or dissimilatory reduction. Whereas Mn(II)-oxidizing bacteria are known to promote indirect oxidation of Cr(III) to Cr(VI), the reaction mechanisms are unresolved. Conversely, oxygen (O2), nitrate (NO3 −), and nitrite (NO2 −) do not appear to play any role in Cr(III) oxidation. Additionally, Mn(II) and ammonium (NH4 +) are not known to promote Cr(VI) reduction. Once reduced, the mobility of Cr(III) in sediments is significantly restricted and regulated by precipitation and sorption processes. Finally, even if the role of natural organic matter in sediment has been determined, further research is required to identify the complexation mechanisms.

Dinitrogen (N2) was reduced to ammonia at room temperature and 1 atmosphere with molybdenum catalysts that contain tetradentate$[HIPTN_{3}N]^{3-}$-triamidoamine ligands {such as$[HIPTN_{3}N]Mo(N_2)$, where$[HIPTN_{3}N]^{3-}$is$[\\{3,5-(2,4,6-i-Pr_{3}C_{6} H_2)_{2}C_{6}H_{3}NCH_{2}CH_2\\}_3N]^{3-}$} in heptane. Slow addition of the proton source$[\\{2,6-lutidinium\\} \\{BAr'_4\\}]$, where Ar' is$3,5-(CF_3)_{2}C_{6}H_3$] and reductant (decamethyl chromocene) was critical for achieving high efficiency (~66% in four turnovers). Numerous x-ray studies, along with isolation and characterization of six proposed intermediates in the catalytic reaction under noncatalytic conditions, suggest that N2was reduced at a sterically protected, single molybdenum center that cycled from Mo(III) through Mo(VI) states.

Impaired Mitochondrial Substrate Oxidation in Muscle of Insulin-Resistant Offspring of Type 2 Diabetic Patients Douglas E. Befroy 1 , Kitt Falk Petersen 1 , Sylvie Dufour 2 , Graeme F. Mason 3 , Robin A. de Graaf 3 , Douglas L. Rothman 3 and Gerald I. Shulman 1 2 4 1 Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 2 Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 3 Department of Diagnostic Radiology, Yale University School of Medicine, New Haven, Connecticut 4 Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut Address correspondence and reprint requests to Gerald I. Shulman, MD, PhD, Howard Hughes Medical Institute, Yale University School of Medicine, The Anlyan Center, S269, P.O. Box 9812, New Haven, CT 06536-8012. E-mail: gerald.shulman{at}yale.edu Abstract Insulin resistance is the best predictor for the development of diabetes in offspring of type 2 diabetic patients, but the mechanism responsible for it remains unknown. Recent studies have demonstrated increased intramyocellular lipid, decreased mitochondrial ATP synthesis, and decreased mitochondrial density in the muscle of lean, insulin-resistant offspring of type 2 diabetic patients. These data suggest an important role for mitochondrial dysfunction in the pathogenesis of type 2 diabetes. To further explore this hypothesis, we assessed rates of substrate oxidation in the muscle of these same individuals using 13 C magnetic resonance spectroscopy (MRS). Young, lean, insulin-resistant offspring of type 2 diabetic patients and insulin-sensitive control subjects underwent 13 C MRS studies to noninvasively assess rates of substrate oxidation in muscle by monitoring the incorporation of 13 C label into C 4 glutamate during a [2- 13 C]acetate infusion. Using this approach, we found that rates of muscle mitochondrial substrate oxidation were decreased by 30% in lean, insulin-resistant offspring (59.8 ± 5.1 nmol · g −1 · min −1 , P = 0.02) compared with insulin-sensitive control subjects (96.1 ± 16.3 nmol · g −1 · min −1 ). These data support the hypothesis that insulin resistance in skeletal muscle of insulin-resistant offspring is associated with dysregulation of intramyocellular fatty acid metabolism, possibly because of an inherited defect in the activity of mitochondrial oxidative phosphorylation. COX, cytochrome oxidase FID, free induction decay IMCL, intramyocellular lipid IRS-1, insulin receptor substrate-1 ISI, insulin sensitivity index MRS, magnetic resonance spectroscopy PDH, pyruvate dehydrogenase PGC, peroxisome proliferator–activated receptor-γ coactivator SDH, succinate dehydrogenase TCA, tricarboxylic acid Footnotes Published ahead of print at http://diabetes.diabetesjournals.org on 7 February 2007. DOI: 10.2337/db06-0783. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Accepted January 31, 2007. Received July 6, 2006. DIABETES

A single bout of exercise can result in inflammatory responses, increased oxidative stress and upregulation of enzymatic antioxidant mechanisms. Although low-volume high-intensity interval training (HIIT) has become popular, its acute responses on the above mechanisms have not been adequately studied. The present study evaluated the effects of HIIT on hematological profile and redox status compared with those following traditional continuous aerobic exercise (CET). Twelve healthy young men participated in a randomized crossover design under HIIT and CET. In HIIT session, participants performed four 30-sec sprints on a cycle-ergometer with 4 min of recovery against a resistance of 0.375 kg/kg of body mass. CET consisted of 30-min cycling on a cycle-ergometer at 70% of their VO . Blood was drawn at baseline, immediately post, 24h, 48h and 72h post-exercise and was analyzed for complete blood count and redox status (thiobarbituric acid reactive substances, [TBARS]; protein carbonyls, [PC]; total antioxidant capacity, [TAC]; catalase and uric acid). White blood cells (WBC) increased after both exercise protocols immediately post-exercise (HIIT: 50% and CET: 31%, respectively). HIIT increased (+22%) PC post-exercise compared to baseline and CET (p < 0.05). HIIT increased TAC immediately post-exercise (16%) and at 24h post-exercise (11%, p < 0.05), while CET increased TAC only post-exercise (12%, p < 0.05) compared to baseline, and TAC was higher following HIIT compared to CET (p < 0.05). Both HIIT and CET increased uric acid immediately post- (21% and 5%, respectively, p < 0.05) and 24h (27% and 5%, respectively, p < 0.05) post-exercise and the rise was greater following HIIT (p < 0.05). There were no significant changes (p > 0.05) for TBARS and catalase following either exercise protocol. Low-volume HIIT is associated with a greater acute phase leukocyte count and redox response than low-volume CET, and this should be considered when an exercise training program is developed and complete blood count is performed for health purposes.

The response of the ocean redox state to the rise of atmospheric oxygen about 2.3 billion years ago (Ga) is a matter of controversy. Here we provide iron isotope evidence that the change in the ocean iron cycle occurred at the same time as the change in the atmospheric redox state. Variable and negative iron isotope values in pyrites older than about 2.3 Ga suggest that an iron-rich global ocean was strongly affected by the deposition of iron oxides. Between 2.3 and 1.8 Ga, positive iron isotope values of pyrite likely reflect an increase in the precipitation of iron sulfides relative to iron oxides in a redox stratified ocean.

Oxygenated organic molecules (OOMs), generated from the oxidation of various biogenic volatile organics with diverse yields, are a great contributor to SOA formation. Terpinolene is an isomeride of limonene, with a high SOA yield. Herein, we investigated the elaborate oxidation mechanism of terpinolene by OH and NO.sub.3, elucidating the new formation mechanism of OOMs and their yield profiles based on the newly-built zero-dimensional chemical model under three typical atmospheric conditions. For terpinolene oxidation by OH, H shift imposes restrictions on continuous autoxidation, instead by the reactions with HO.sub.2 /NO/NO.sub.2 resulting in chain termination. For the reaction of terpinolene with NO.sub.3, the transfer of the radical center via bond breaking, triggering a new round of autoxidation, is newly found to be pivotal in the formation of organic nitrate (RONO.sub.2) OOMs with high yields. The effective saturation concentration (C.sup.â) of RONO.sub.2 OOMs is mostly lower than the OOMs formed by OH oxidation, more easily distributed into the particle phase. The estimated C.sup.â of the generated OOMs is distinctly varied among OOM isomers, which emphasizes the necessity of determining their molecular structures, peculiarly the number of rings. The comparative analysis of OH-initiated (daytime) and NO.sub.3 -driven (nocturnal) terpinolene oxidation mechanism, highlighted the formation of RONO.sub.2 OOMs, would be conducive to molecular structure identification of OOMs in atmospheric monitoring and atmospheric chemical model refinement.

Lipid metabolism is important for health and insulin action, yet the fundamental process of regulating lipid metabolism during muscle contraction is incompletely understood. Here, we show that liver kinase B1 (LKB1) muscle-specific knockout (LKB1 MKO) mice display decreased fatty acid (FA) oxidation during treadmill exercise. LKB1 MKO mice also show decreased muscle SIK3 activity, increased histone deacetylase 4 expression, decreased NAD+ concentration and SIRT1 activity, and decreased expression of genes involved in FA oxidation. In AMP-activated protein kinase (AMPK)α2 KO mice, substrate use was similar to that in WT mice, which excluded that decreased FA oxidation in LKB1 MKO mice was due to decreased AMPKα2 activity. Additionally, LKB1 MKO muscle demonstrated decreased FA oxidation in vitro. A markedly decreased phosphorylation of TBC1D1, a proposed regulator of FA transport, and a low CoA content could contribute to the low FA oxidation in LKB1 MKO. LKB1 deficiency did not reduce muscle glucose uptake or oxidation during exercise in vivo, excluding a general impairment of substrate use during exercise in LKB1 MKO mice. Our findings demonstrate that LKB1 is a novel molecular regulator of major importance for FA oxidation but not glucose uptake in muscle during exercise.

In type 2 diabetes, hyperglycemia and increased sympathetic drive may alter mitochondria energetic/redox properties, decreasing the organelle’s functionality. These perturbations may prompt or sustain basal low-cardiac performance and limited exercise capacity. Yet the precise steps involved in this mitochondrial failure remain elusive. Here, we have identified dysfunctional mitochondrial respiration with substrates of complex I, II, and IV and lowered thioredoxin-2/glutathione (GSH) pools as the main processes accounting for impaired state 4→3 energetic transition shown by mitochondria from hearts of type 2 diabetic db/db mice upon challenge with high glucose (HG) and the β-agonist isoproterenol (ISO). By mimicking clinically relevant conditions in type 2 diabetic patients, this regimen triggers a major overflow of reactive oxygen species (ROS) from mitochondria that directly perturbs cardiac electro-contraction coupling, ultimately leading to heart dysfunction. Exogenous GSH or, even more so, the fatty acid palmitate rescues basal and β-stimulated function in db/db myocyte/heart preparations exposed to HG/ISO. This occurs because both interventions provide the reducing equivalents necessary to counter mitochondrial ROS outburst and energetic failure. Thus, in the presence of poor glycemic control, the diabetic patient’s inability to cope with increased cardiac work demand largely stems from mitochondrial redox/energetic disarrangements that mutually influence each other, leading to myocyte or whole-heart mechanical dysfunction.

The insertion of an iridium complex into an N-H bond in ammonia leads to a stable monomeric amido hydride complex in solution at room temperature. This reaction advances the transition-metal coordination chemistry of ammonia beyond its role for more than a century as an ancillary ligand. The precursor for this insertion reaction is an iridium(I) olefin complex with an aliphatic ligand containing one carbon and two phosphorus donor atoms. Kinetic and isotopic labeling studies indicate that olefin dissociates to give a 14-electron iridium(I) fragment, which then reacts with ammonia. This cleavage of the N-H bond under neutral conditions provides a foundation on which to develop future mild catalytic transformations of ammonia, such as olefin hydroamination and arene oxidative amination.