A process-orientated design and performance assessment methodology for passive mine water treatment systems

The aim of this paper is the development of a methodology for assessing the iron removal efficiency of passive mine water treatment settling lagoons and reed beds. Previous work in the design and sizing of coal mine drainage lagoons and wetlands has focussed on the use of standard hydraulic residence times or using the 10 g m⁻² d⁻¹ metric, these criteria have been applied without regard to the fundamental physical and chemical processes controlling iron removal in the system, namely the pH dependent rates of Fe(II) oxidation and physical settling of the particulate Fe(III). In this study field water quality data have been collected from lagoons and reed beds. These data are examined alongside data from the UK Coal Authority database and combined with simple mathematical formulations to provide a framework through which to understand passive treatment schemes from a process-orientated perspective. It is demonstrated that for the sites studied reed beds are more efficient for iron removal. This paper recommends that judgements of iron removal performance should be based on a derived treatment efficiency index (?) and that the modelling approach espoused in this paper should be used when designing passive mine water treatment schemes.     

Flux of reduced chemical constituents (Fe2+, Mn2+, NH inf4 sup+ and CH4) and sediment oxygen demand in Lake Erie

Sediment pore water concentrations of Fe²⁺, Mn²⁺, NH _inf4 ^sup+ and CH₄ were analyzed from both diver-collected cores and anin situ equilibration device (peeper) in Lake Erie's central basin. Sediment oxygen demand (SOD) was measured at the same station with a hemispheric chamber (including DO probe and recorder) subtending a known area of sediments. The average SOD was 9.4 mM m⁻² day⁻¹ (0.3 g m⁻² day⁻¹). From pore water gradients within the near-surface zone, the chemical flux across the interface was calculated indirectly using Fick's first law modified for sediments. These calculations, using core and peeper gradients, always showed sediment loss to overlying waters, and variations between the two techniques differed by less than an order of magnitude for Fe²⁺ and CH₄. The transport of these reduced constituents can represent a sizeable oxygen demand, ranging from less than 1% for Fe²⁺ and Mn²⁺ to as high as 26% for NH _inf4 ^sup+ , and 30% for CH₄. The average flux of these constituents could account for about a third of the SOD at the sediment-water interface of this station.     

Impacts of ISCO Persulfate,Peroxide and Permanganate Oxidants on Soils: Soil Oxidant Demand and Soil Properties

The consumption of in-situ chemical oxidation (ISCO) oxidant by soil oxidizable matter (OM), termed the soil oxidant demand (SOD), is an essential factor when designing treatments for successful remediation at an ISCO site. This study aims to assess the impact of different oxidants on SOD and the soil itself, using the Taguchi experimental design. Five oxidation systems, including persulfate (PS), hydrogen peroxide (HP), permanganate (PM), Fe²⁺ activated PS and Fe²⁺ activated HP, and four factors including oxidant concentration, activator concentration, reaction time, and pH were investigated. The results of the Taguchi analysis in this study show that oxidant concentration had the greatest effect on the SOD. Other factors also affected the SOD and the optimum conditions for achieving a lower SOD were determined using the Taguchi design method. Additionally, original and oxidized soils were analyzed using a scanning electron microscope equipped with an X-ray energy dispersive spectrometer to determine the surface morphology and chemical composition of the samples. Variations in soil organic carbon levels and total soil bacterial counts were recorded and the speciation of soil minerals (Fe, Mn, Cu, and Zn) was analyzed.     

The SGLT2 inhibitor dapagliflozin promotes systemic FFA mobilization,enhances hepatic β-oxidation,and induces ketosis

Sodium-glucose cotransporter 2 (SGLT2) inhibitors have been shown to increase ketone bodies in patients with type 2 diabetes; however, the underlying mechanisms have not been fully elucidated. Here we examined the effect of the SGLT2 inhibitor dapagliflozin (1 mg/kg/day, formulated in a water, PEG400, ethanol, propylene glycol solution, 4 weeks) on lipid metabolism in obese Zucker rats. Fasting FFA metabolism was assessed in the anesthetized state using a [9,10-³H(N)]-palmitic acid tracer by estimating rates of plasma FFA appearance (R_a), whole-body FFA oxidation (R_ox), and nonoxidative disposal (R_st). In the liver, clearance (K_β-ox) and flux (R_β-ox) of FFA into β-oxidation were estimated using [9,10-³H]-(R)-bromopalmitate/[U-¹⁴C]palmitate tracers. As expected, dapagliflozin induced glycosuria and a robust antidiabetic effect; treatment reduced fasting plasma glucose and insulin, lowered glycated hemoglobin, and increased pancreatic insulin content compared with vehicle controls. Dapagliflozin also increased plasma FFA, R_a, R_ox, and R_st with enhanced channeling toward oxidation versus storage. In the liver, there was also enhanced channeling of FFA to β-oxidation, with increased K_β-ox, R_β-ox and tissue acetyl-CoA, compared with controls. Finally, dapagliflozin increased hepatic HMG-CoA and plasma β-hydroxybutyrate, consistent with a specific enhancement of ketogenesis. Since ketogenesis has not been directly measured, we cannot exclude an additional contribution of impaired ketone body clearance to the ketosis. In conclusion, this study provides evidence that the dapagliflozin-induced increase in plasma ketone bodies is driven by the combined action of FFA mobilization from adipose tissue and diversion of hepatic FFA toward β-oxidation.     

Effect of temperature on the pathways of NADH-oxidation in broad-bean mitochondria

1. Respiration rates of broad-bean (Vicia faba) mitochondria were studied as a function of temperature. Arrhenius plots of all membrane-bound enzymes, as obtained with saturating substrate concentrations, revealed a break in the lower temperature range. That break was considered to indicate a phase transition of membrane phospholipids, characteristic for chilling-sensitive plants. A second discontinuity at 30°C occurred only with activities linked to energy conservation. — 2. The activation energies for the oxidation of NAD⁺-linked substrates differ between states 3 and 4. State 3 respiration of NAD⁺-linked substrates is the result a superimposition of two branches of electron transport, which can be separated by different sensibilities to rotenone. A characteristic temperature dependency of the respiratory control, as well as a shift of the low temperature break in the Arrhenius plot toward a higher temperature after state 4 to state 3 transition, are calculated to be caused by the superimposition of the two branches. — 3. The temperature dependency of the oxidation of extra-mitochondrial NADH and of succinate differs remarkably from that of the oxidation of matrix-NADH. It has been concluded that the rotenone-resistant oxidation of matrix-NADH and the oxidation of external NADH are mediated via different pathways with individual regulation sites.Abbreviations BSA bovine serum albumin - CCCP carbonylcyanide-m-chlorophenylhydrazone - TPP thiaminepyrophosphate     

Desferrioxamine as an Electron Donor. Inhibition of Membranal Lipid Peroxidation Initiated by H202 –Activated Metmyoglobin and Other Peroxidizing Systems

Desferoxamine (DFO) involvement in several peroxidative systems was studied. These sytems included: a) membranal lipid peroxidation initiated by H₂O₂-activated metmyoglobin (or methemoglobin); b) phenol-red oxidation by activated metmyoglobin or horseradish peroxidase (HRP): c) β-carotene-linoleate couple oxidation stimulated by lipoxygenase or hemin. Desferrioxamine was found to inhibit all these systems but not ferrioxamine (FO). Phenol-red oxidation by H₂0₂-horseradish peroxidase was inhibited competitively with DFO. Kinetic studies using the spectra changes in the Soret region of metmyoglobin suggest a mechanism by which H₂0₂ reacts with the iron-heme to form an intermediate of oxy-ferryl myoglobin that subsequently reacts with DFO to return the activated compound to the resting state. These activities of DFO resemble the reaction of other electron donors.     

Effect of cultural conditions on the lipid profile of Thiobacillus ferroxidas

The intensitive investigations on the lipid profile of Thiobacillus ferrooxidans at various culture ages suggest some correlations of the lipid constitutents with the membrane-bound iron oxidation system. Phosphatidic acid, phosphatidyl serine and phosphatidyl ethanolamine were the major polar components; hydrocarbon, triglyceride and diglyceride were the main neutral components. Major fatty acids were C_16:0, C_16:1, C_16:3, C_18:1, C_18:3, C_22:1 while C_20:1, C_20:2, C_12:0, C_14:2, C_18:0, C_18:2, C_20:0, C_22:0 were found in trace amounts which also depended upon the phase of the growth. One lipoamino acid was identified as ornithine lipid in the polar fraction. Each and every component varied to some extent at different growth phasesindicating relationship of these lipids to the iron oxidation system of the strain.     

Dysfunction of rat liver mitochondria by selenite: induction of mitochondrial permeability transition through thiol-oxidation

Selenium is an essential trace element in mammals and is thought to play a chemopreventive role in human cancer, possibly by inducing tumor cell apoptosis. Mitochondria play a pivotal role in the induction of apoptosis in many cell types. The effects of selenite on mitochondrial function were therefore investigated. Selenite induced the oxidation and cross-linking of protein thiol groups, mitochondrial permeability transition (MPT), a decrease in the mitochondrial membrane potential, and the release of cytochrome c in mitochondria isolated from rat liver. Induction of the MPT by selenite was prevented by cyclosporin A, EGTA, or N-ethylmaleimide. These results thus indicate that selenite induces the MPT as a result of direct modification of protein thiol groups, resulting in the release of cytochrome c and a loss of mitochondrial membrane potential.     

Inhibition of ozone-induced SP-A oxidation by plant polyphenols

Surfactant protein-A (SP-A) is the best studied and most abundant of the protein components of lung surfactant and plays an important role in host defense of the lung. It has been shown that ozone-induced oxidation of SP-A protein changes its functional and biochemical properties. In the present study, eight plant polyphenols (three flavonoids, three hydroxycinnamic acids, and two hydroxybenzoic acids) known as strong antioxidants, were tested for their ability to inhibit ozone-induced SP-A oxidation as a mechanism for chemoprevention against lung damage. SP-A isolated from alveolar proteinosis patients was exposed to ozone (1 ppm) for 4 h. The flavonoids protected SP-A from oxidation in a dose dependent manner. ( - )-Epicatechin was the most potent flavonoid and exhibited inhibition of ozone-induced formation of carbonyls by 35% at a concentration as low as 5 μM. Hydroxybenzoic acids inhibited SP-A oxidation in a dose-dependent manner although they were less potent than flavonoids. On the other hand, hydroxycinnamic acids exhibited a different inhibitory pattern. Inhibition was observed only at medium concentrations. The results indicate that inhibition of SP-A oxidation by plant polyphenols may be a mechanism accounting for the protective activity of natural antioxidants against the effects of ozone exposure on lungs.     

Subcellular distribution,molecular dynamics and catabolism of plasmalogens in myocardium

Recent studies have implicated accelerated sarcolemmal phospholipid catabolism as a mediator of the lethal sequelae of atherosclerotic heart disease. We have demonstrated that plasmalogens are the predominant phospholipid constituents of canine myocardium and that plasmalogens are hydrolyzed by a novel calcium independent plasmalogen selective phospholipase A2. Since the activities of phospholipases are modulated by the molecular dynamics and interfacial characteristics of their phospholipid substrates, we compared the molecular dynamics of plasmenylcholine and phosphatidylcholine vesicles by electron spin resonance spectroscopy and deuterium magnetic resonance spectroscopy. Plasmenylcholine vesicles have separate and distinct molecular dynamics in comparisons to their phosphatidylcholine counterparts as ascertained by substantial decreases in the angular fluctuations and motional velocities of probes attached to their sn-2 aliphatic constituents. Furthermore, since free radical oxidation of myocardial lipid constituents occurs during myocardial ischemia and reperfusion, we demonstrated that ¹O₂ mediated oxidation of plasmenylcholine resulted in the generation of several products which have chromatographic characteristics and molecular masses corresponding to 2-acyl lysophosphatide derivatives. Taken together, these studies underscore the biologic significance of the predominance of sarcolemmal plasmalogens present in mammalian myocardium and suggest that their catabolism by plasmalogen selective phospholipases and/or oxidative processes may contribute to the lethal sequelae of myocardial ischemia.