ABSTRACT
Carbon mineralization processes and their dependence on environmental conditions (e.g. through macrobenthic bioturbation) have been widely studied in temperate coastal sediments, but almost nothing is known about these processes in subtropical coastal sediments. This study investigated pathways of organic carbon mineralization and associated effects of macrobenthic bioturbation in winter and summer (September 2012 and February 2014) at the SE Brazilian coast. Iron reduction (FeR) was responsible for 73-81% of total microbial carbon mineralization in September 2012 and 32-61% in February 2014. Similar high rates of FeR have only been documented a few times in coastal sediments and can be sustained by the presence of large bioturbators. Denitrification accounted for 5-27% of total microbial carbon mineralization while no SO4(2-) reduction was detected in any season. Redox profiles suggested that conditions were less reduced in February 2014 than in September 2012, probably associated with low reactivity of the organic matter, higher rates of aerobic respiration and bioirrigation by the higher density of small-macrofauna. Bioturbation by small macrofauna may maintain the sediment oxidized in summer, while large-sized species stimulate the reoxidation of reduced compounds throughout the year. Therefore, bioturbation seems to have an important role modulating the pathways of carbon mineralization in the area.
Subject(s)
Carbon/metabolism , Geologic Sediments/chemistry , Ammonium Compounds/chemistry , Ammonium Compounds/metabolism , Brazil , Bromides/chemistry , Bromides/metabolism , Carbon Dioxide/chemistry , Carbon Dioxide/metabolism , Iron/chemistry , Nitrates/chemistry , Nitrates/metabolism , Oxidation-Reduction , Oxygen/chemistry , Seasons , Seawater/chemistry , Seawater/microbiologyABSTRACT
Dihydrolipoamide dehydrogenase (LADH) lipoamide reductase activity decreased whereas enzyme diaphorase activity increased after LADH treatment with myeloperoxidase (MPO) dependent systems (MPO/H2O2/halide, MPO/NADH/halide and MPO/H2O2/nitrite systems. LADH inactivation was a function of the composition of the inactivating system and the incubation time. Chloride, iodide, bromide, and the thiocyanate anions were effective complements of the MPO/H2O2 system. NaOCl inactivated LADH, thus supporting hypochlorous acid (HOCl) as putative agent of the MPO/H2O2/NaCl system. NaOCl and the MPO/H2O2/NaCl system oxidized LADH thiols and NaOCl also oxidized LADH methionine and tyrosine residues. LADH inactivation by the MPO/NADH/halide systems was prevented by catalase and enhanced by superoxide dismutase, in close agreement with H2O2 production by the LADH/NADH system. Similar effects were obtained with lactoperoxidase and horse-radish peroxidase supplemented systems. L-cysteine, N-acetylcysteine, penicillamine, N-(2-mercaptopropionylglycine), Captopril and taurine protected LADH against MPO systems and NaOCl. The effect of the MPO/H2O2/NaNO2 system was prevented by MPO inhibitors (sodium azide, isoniazid, salicylhydroxamic acid) and also by L-cysteine, L-methionine, L-tryptophan, L-tyrosine, L-histidine and reduced glutathione. The summarized observations support the hypothesis that peroxidase-generated "reactive species" oxidize essential thiol groups at LADH catalytic site.
Subject(s)
Dihydrolipoamide Dehydrogenase/antagonists & inhibitors , Myocardium/enzymology , Peroxidase/metabolism , Sodium Nitrite/metabolism , Sulfhydryl Compounds/metabolism , Amino Acids/pharmacology , Animals , Binding Sites , Bromides/metabolism , Catalase/metabolism , Chlorides/metabolism , Dihydrolipoamide Dehydrogenase/metabolism , Humans , Hydrogen Peroxide/metabolism , Hydrogen-Ion Concentration , Hypochlorous Acid/pharmacology , Iodides/metabolism , Peroxidase/antagonists & inhibitors , Superoxide Dismutase/metabolism , Swine , Taurine/pharmacology , Thiocyanates/metabolismABSTRACT
Body water compartment changes were assessed during postnatal weight loss in 14 infants with respiratory distress syndrome. Total body water and extracellular volume were measured by dilution methods on the first day of life and again between the third and sixth days of life. Extracellular volume changes were calculated between the first and second determinations by measurement of chloride balance. Fluid therapy was prescribed to allow negative net water balance and a 1% to 3% reduction in body weight per day. All infants had concurrent reductions in body weight, total body water, and extracellular volume. Progressive daily extracellular volume reduction concurrent with weight loss was also apparent from chloride balance data. The correlation of changes in body weight with extracellular volume in individual subjects was poor (r = 0.05). We speculate that variations between sodium and free water balance in the sick preterm infant may be responsible for variability in the distribution of postnatal body water losses. Assessment of hydration in the newborn infant should include consideration of sodium balance and alterations of serum osmolality, and changes in body weight.