Concomitant Chloride Research Articles

Dichloromethane biodegradation in multi-contaminated groundwater: Insights from biomolecular and compound-specific isotope analyses

Dichloromethane (DCM) is a widespread and toxic industrial solvent which often co-occurs with chlorinated ethenes at polluted sites. Biodegradation of DCM occurs under both oxic and anoxic conditions in soils and aquifers. Here we investigated in situ and ex situ biodegradation of DCM in groundwater sampled from the industrial site of Themeroil (France), where DCM occurs as a major co-contaminant of chloroethenes. Carbon isotopic fractionation (εC) for DCM ranging from −46 to −22‰ were obtained under oxic or denitrifying conditions, in mineral medium or contaminated groundwater, and for laboratory cultures of Hyphomicrobium sp. strain GJ21 and two new DCM-degrading strains isolated from the contaminated groundwater. The extent of DCM biodegradation (B%) in the aquifer, as evaluated by compound-specific isotope analysis (δ13C), ranged from 1% to 85% applying DCM-specific εC derived from reference strains and those determined in this study. Laboratory groundwater microcosms under oxic conditions showed DCM biodegradation rates of up to 0.1 mM·day−1, with concomitant chloride release. Dehalogenase genes dcmA and dhlA involved in DCM biodegradation ranged from below 4 × 102 (boundary) to 1 × 107 (source zone) copies L−1 across the contamination plume. High-throughput sequencing on the 16S rrnA gene in groundwater samples showed that both contaminant level and terminal electron acceptor processes (TEAPs) influenced the distribution of genus-level taxa associated with DCM biodegradation. Taken together, our results demonstrate the potential of DCM biodegradation in multi-contaminated groundwater. This integrative approach may be applied to contaminated aquifers in the future, in order to identify microbial taxa and pathways associated with DCM biodegradation in relation to redox conditions and co-contamination levels.

Molecular Characterization of Monochloroacetate-Degrading Arthrobacter sp. Strain D2 Isolated from Universiti Teknologi Malaysia Agricultural Area

ABSTRACT Arthrobacter sp. strains D2 and D3 and Labrys sp. strain D1 capable of degrading 20 mM monochloroacetic acid (MCA) were isolated from soil contaminated with herbicides and pesticides. All three isolates were able to grow on MCA as the sole source of carbon and energy with concomitant chloride ion release in the growth medium (19 mM). Strains D2 and D3 (cells doubling time 7 ± 0.3 h) grew four times faster than D1 (26 ± 0.1 h). Strain D2 was then further investigated and could also grow in 10 mM of monobromoacetic acid (MBA), 2,2-dichloropropionic acid (2,2DCP), d,l-2-chloropropionic acid (D,L2CP), l-2-chloropropionic acid (L-2CP), d-2-chloropropionic acid (D-2CP), and glycolate as the sole sources of carbon and energy. Dehalogenase gene amplification using group I primers revealed a 410-bp polymerase chain reaction (PCR) product, but there was none using group II primers. The partial amino acid sequence analysis of group I DehD2 dehalogenase showed at least 32% identity to the corresponding regions of DehE, DhlIV, DehI, and D,L-DEX, with key amino acid residues Ser188, Ala187, and Asp189. These amino acid residues were involved in substrate binding and catalysis and were conserved in the partial amino acid sequence.

Dehalogenation of environmental pollutants in microbial electrolysis cells with biogenic palladium nanoparticles

Hydrodehalogenation of persistent pollutants, such as the groundwater contaminants trichloroethylene and diatrizoate, are catalyzed by biogenic Pd nanoparticles. As H(2) gas supply for the dehalogenation reactions is still the limiting factor, this study examines in situ H(2) production in the cathode of a microbial electrolysis cell. In a biogenic Pd nanoparticle (bio-Pd) free microbial electrolysis cell (MEC), dechlorination of trichloroethylene (TCE) with concomitant chloride and ethane formation was achieved in the cathode compartment at a removal rate of 120 g TCE m(-3) total cathode compartment (TCC) day(-1), applying -0.8 V with a power source. When the cathode granules were coated with 5 mg bio-Pd g(-1) graphite, chloride and ethane formation increased to 151 g TCE m(-3) TCC day(-1) corresponding with a specific removal rate of 48 mg TCE g(-1) Pd day(-1). In both cases, formation of unwanted byproducts, such as vinyl chloride, was not significant. When the same setup was applied for transformation of the iodinated contrast medium diatrizoate (diaI(3)), reduction in a catalyst-free cathode of a MEC resulted in a removal of 48 ± 9% during the first h corresponding to 3 g diaI(3) m(-3) TCC day(-1). Coating the cathodic graphite granules with bio-Pd enhanced the transformation resulting in a 93 ± 4% removal during the first h corresponding to 6 g diaI(3) m(-3) TCC day(-1). These results suggest that MECs can produce H(2) in a sustainable way to provide an economical interesting reactant for bio-Pd catalyzed dehalogenation reactions.

Electrophysiology of Reactive Oxygen Production in Signaling Endosomes

Endosome trafficking and function require acidification by the vacuolar ATPase (V-ATPase). Electrogenic proton (H+) transport reduces the pH and creates a net positive charge in the endosomal lumen. Concomitant chloride (Cl-) influx has been proposed to occur via ClC Cl-=H+ exchangers. This maintains charge balance and drives Cl- accumulation, which may itself be critical to endosome function. Production of reactive oxygen species (ROS) in response to cytokines occurs within specialized endosomes that form in response to receptor occupation. ROS production requires an NADPH oxidase (Nox) and the ClC-3 Cl-=H+ exchanger. Like the V-ATPase, Nox activity is highly electrogenic, but separates charge with an opposite polarity (lumen negative). Here we review established paradigms of early endosomal ion transport focusing on the relation between the V-ATPase and ClC proteins. Electrophysiologic constraints on Nox-mediated vesicular ROS production are then considered. The potential for ClC-3 to participate in charge neutralization of both proton (V-ATPase) and electron (Nox) transport is discussed. It is proposed that uncompensated charge separation generated by Nox enzymatic activity could be used to drive secondary transport into negatively charged vesicles. Further experimentation will be necessary to establish firmly the biochemistry and functional implications of endosomal ROS production.

A New Family of Acylrhodium Organometallics

The Schiff mono bases of 2,6-diformyl-4-methylphenol, 1, react with RhCl3·3H2O and PPh3 in ethanol, affording dichloro[4-methyl-6-((arylimino)methyl)phenolato-C1,O]bis(triphenylphosphine)rhodium(III), Rh(XLsb)(PPh3)2Cl2 (5; X = H, Me, OMe, Cl). Organometallics of the type (carboxylato)[4-methyl-6-formylphenolato-C1,O]bis(triphenylphosphine)rhodium(III), Rh(Lal)(PPh3)2(RCO2) (6; R = H, Me, Et, Ph), have been synthesized by oxidative addition of 1 to RhCl(PPh3)3 in the presence of dilute RCO2H in ethanol. Replacement of RCO2H by dilute HNO3 has afforded the nitrate analogue Rh(Lal)(PPh3)2(NO3) (7). Species of type 5 are susceptible to aldiminium → aldehyde hydrolysis in a dichloromethane−acetone−water mixture with concomitant chloride dissociation, furnishing Rh(Lal)(PPh3)2Cl (8a), from which the N-bonded nitrite Rh(Lal)(PPh3)2(NO2) (8b) has been generated metathetically. The four types of species 5−8 are interconvertible, and a possible reaction pathway involving pentacoordinate intermediates is proposed. ...

Genetic and biochemical characterization of the broad spectrum chlorobenzene dioxygenase from Burkholderia sp. strain PS12--dechlorination of 1,2,4,5-tetrachlorobenzene.

The bacterium, Burkholderia (previously Pseudomonas) sp. strain PS12, reported earlier to degrade 1,2,4-trichlorobenzene is shown here to utilize also 1,2,4,5-tetrachlorobenzene (Cl4-benzene) as a growth substrate. To investigate the possibility that this organism attacks Cl4-benzene with a chlorobenzene dioxygenase which concomitantly causes dehalogenation, and to analyze the substrate range of the initial enzyme, a 5503-bp DNA fragment from PS12, exhibiting high similarity to genes coding for class IIB dioxygenases, was cloned and expressed in Escherichia coli. The sequence includes the tec genes coding for the alpha-subunit and beta-subunit of a terminal dioxygenase, a ferredoxin and a reductase. E. coli cells producing these proteins were able to dioxygenolytically attack a range of aromatic compounds including chlorinated benzenes and toluene, and also dinuclear aromatics such as biphenyl and dibenzo-p-dioxin. The enzyme was shown by (18)O2 incorporation experiments to dioxygenolytically attack a chlorosubstituted carbon atom of Cl4-benzene, thereby forming an unstable diol intermediate which spontaneously rearomatizes with concomitant chloride elimination to the corresponding 3,4,6-trichlorocatechol (Cl3-catechol).

Biodegradation of 3,4‐dichloroaniline in a fluidized bed bioreactor and a steady‐state biofilm Kinetic model

Mixed culture of microorganisms immobilized onto Celite diatomaceous earth particles were used to degrade 3,4-dichloroaniline (34DCA) in a three-phase draft tube fluidized bed bioreactor. Biodegradation was confirmed as the dominant removal mechanism by measurements of the concomitant chloride ion evolution. Degradation efficiencies of 95% were obtained at a reactor retention time of 1.25 h. A mathematical model was used to describe the simultaneous diffusion and reaction of 34DCA and oxygen in the biofilms on the particles in the reactor. The parameters describing freely suspended cell growth on 34DCA were obtained in batch experiments. The model was found to describe the system well for three out of four steady states and to predict qualitatively the experimentally observed transition in the biofilm kinetics from 34DCA to oxygen limitation.

Potassium-depletion alkalosis in the rat.

Studies were performed to investigate the role of concomitant chloride depletion in potassium-depletion alkalosis in the rat and the relationship between potassium depletion, plasma bicarbonate (PHCO3), and net acid excretion. 1) Selective potassium depletion (K-DEPL), potassium plus chloride depletion (KCl-DEPL), or selective chloride depletion (Cl-DEPL) was produced by administering a selectively potassium-, potassium and chloride-, or selectively chloride-deficient diet. In K-DEPL and KCl-DEPL rat, PHCO3 increased progressively and similarly during a 38-day period of restriction, whereas net acid excretion was similar and not elevated in either group. Cl-DEPL did not result in alkalosis. Chloride administration without potassium in alkalotic KCl-DEPL rats did not result in a sustained significant decrease in PHCO3. Potassium administration without chloride in alkalotic KCl-DEPL rats decreased PHCO3. Thus concomitant chloride depletion plays a minimal role in the alkalosis produced by dietary-induced potassium depletion. 2) Administration of a chronic acid load to alkalotic K-DEPL rats did not decrease PHCO3, and net acid excretion increased similarly as in normals. In K-DEPL rats after PHCO3 was reduced toward normal levels with acetazolamide, net acid excretion increased sharply above base-line values and PHCO3 increased markedly. Thus the alkalotic K-DEPL rat maintains the ability to excrete a chronic acid load, and a reduction in PHCO3 elicits an increase in acid excretion to restore the initial acid-base condition. These studies suggest that potassium depletion alters the set-point at which the kidney maintains PHCO3.

Cerebral dysfunction following infantile dietary chloride deficiency

Twenty-two children who were chloride-depleted in infancy due to a chloride-deficient diet and who had resultant hypochloremic alkalosis were analyzed in regard to their signs and symptoms, metabolic studies, and growth parameters. Deceleration of weight, linear growth, and head growth occurred in most, and persistent growth failure occurred in some. The majority had cognitive deficits at follow-up. Comparison with growth parameters in a chronically malnourished group of children who had a variety of disorders revealed a similar degree of deceleration of weight (p = 0.50) and height (p = 0.70), but more severe deceleration of head growth (p = 0.01). Comparison with follow-up cognitive deficits reported in the United States medical literature in children with similar severity of nutritional deprivation indicates that the chloride-depleted infants had more frequent and more severe cognitive deficits (p = 0.09). Cognitive deficits have been documented in U.S. children who are nutritionally deprived only when disorders causing concomitant chloride depletion are responsible for the malnutrition.

Effects of acute potassium infusions with salts other than chloride on plasma renin activity.

To evaluate the contribution of chloride to the suppression of plasma renin activity (PRA) by KCl, PRA was measured before and after venous infusions of KCl, KHCO3, KNO3, and KC2H3O2 in dietary NaCl-restricted rats. In contrast to controls, PRA decreased (P less than 0.02) after infusion of each potassium salt [KCl from 55.3 +/- 6.4 to 27.0 +/- 6.4 ng.ml-1.h-1 (mean +/- SE); KC2H3O2 from 39.3 +/- 4.0 to 20.6 +/- 4.0; KHCO3 from 64.4 +/- 6.2 to 47.2 +/- 6.2; KNO3 from 40.0 +/- 4.0 to 18.6 +/- 4.0]. Arterial pressure, plasma volume, inulin clearance, serum sodium concentration, and net sodium balance were not different between control and potassium-infused groups. Potassium loading did not increase absolute or fractional sodium excretion. PRA failed to decrease in animals given an equal volume of NaNO3. Furosemide prevented the fall in PRA associated with potassium loading despite replacement of urinary losses. These results suggest that the decrease in PRA observed during potassium loading occurs through the macula densa mechanism but is not dependent on concomitant chloride administration. As furosemide prevents the fall in PRA, macula densa chloride transport may be necessary for potassium to exert this effect.

The role of the colon in the pathogenesis of hyperchloraemic acidosis in ureterosigmoid anastomosis.

1. The composition of urine-faeces mixture in seven patients with ureterosigmoid anastomosis has been studied by a dialysis in vivo method using cellulose bags. Urine—faeces dialysate obtained from these patients contained much greater amounts of both bicarbonate and total ammonia than has been reported for faecal dialysate in normal subjects. 2. Total ammonia concentrations in urine– faeces specimens obtained by catheter suggest that urine excreted by the kidneys in these patients becomes increasingly acid with increasing systemic acidosis. The highly alkaline nature of urine-faeces mixtures, especially in acidotic patients, indicates rapid alkalinization of the mixture in the colon. It appears that colonic secretion of bicarbonate is a direct consequence of the acidity of urine excreted by the kidney and draining into the colon. 3. The study suggests that the development of hyperchloraemic acidosis in patients with ureterosigmoid anastomosis is due to bicarbonate secretion by the colonic mucosa, with concomitant chloride absorption. With the development of metabolic acidosis, rapid alkalinization of the urine still occurs in the colon, but during further retention of the urine-faeces in the colon some reabsorption of bicarbonate occurs, probably in part by ionic diffusion since chloride concentration in the lumen increases. 4. Evidence suggestive of non-ionic diffusion of ammonia was found in only one patient. It seems probable that higher rates of urea breakdown in other patients mask the expected relationship between total ammonia and bicarbonate.