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PubMed1992

Aerobic vinyl chloride metabolism in Mycobacterium aurum L1.

Mycobacterium aurum L1, capable of growth on vinyl chloride as a sole carbon and energy source, was previously isolated from soil contaminated with vinyl chloride (S. Hartmans et al., Biotechnol. Lett. 7:383-388, 1985). The initial step in vinyl chloride metabolism in strain L1 is catalyzed by alkene monooxygenase, transforming vinyl chloride into the reactive epoxide chlorooxirane. The enzyme responsible for chlorooxirane degradation appeared to be very unstable and thus hampered the characterization of the second step in vinyl chloride metabolism. Dichloroethenes are also oxidized by vinyl chloride-grown cells of strain L1, but they are not utilized as growth substrates. Three additional bacterial strains which utilize vinyl chloride as a sole carbon and energy source were isolated from environments with no known vinyl chloride contamination. The three new isolates were similar to strain L1 and were also identified as Mycobacterium aurum.

Biodegradation, Environmental↗
PubMed1987

The comparative effects of feeding ammonium carbonate, ammonium sulfate, and ammonium chloride on urinary calcium excretion in the rat.

When either sulfate or chloride is added to the diet, the resulting acid load causes a rise in urinary calcium excretion. There is, however, the possibility that sulfate, which has been shown to complex renal tubular calcium, will further decrease renal calcium reabsorption and thus produce a greater calciuria than chloride. Because addition of a fixed cation (e.g., sodium) to the diet may also stimulate calciuresis, experiments were conducted using metabolizable ammonium to minimize cation effects. Ammonium salts of sulfate, chloride, and carbonate (control) were added to the diets of male rats at 0.3 mequiv./g weight of diet. Twenty-four hour excretion rates of calcium, sulfate, chloride, and net acid were measured at various intervals up to 1 month. As expected, the chloride and sulfate diets were both associated with significantly elevated urine calcium and net acid excretion as compared with controls. However, those fed sulfate exhibited significantly less calcium and acid excretion and absorbed a smaller proportion of the anion load than those given chloride. In a second experiment, the amounts of supplemental sulfate and chloride were adjusted so that total absorptions were similar. At 2 weeks, both calcium and acid excretions in the fixed anion groups were no longer significantly different. Thus, in chronic feeding trials, there appears to be no measurable difference in the calciuretic properties of sulfate and chloride anions.

Ammonium Chloride↗
PubMed1988

Chloride transport in the proximal renal tubule.

Our knowledge of chloride transport along the nephron has greatly expanded. Whereas for a long time it was assumed that chloride ions were reabsorbed entirely passively with sodium--the "mendicant" role of chloride, more recent studies suggest that several distinct reabsorptive transport mechanisms operate in parallel. Accordingly, a new model of proximal chloride transport has evolved that includes both active, transcellular as well as passive, intercellular transport pathways. Transcellular chloride reabsorption involves anion exchange mechanisms in both the luminal and peritubular cell membranes, processes that also depend on sodium, hydrogen, and bicarbonate ions. Chloride transport is thus intimately related to sodium and fluid transport as well as to cell acid-base metabolism. Unresolved problems concern the relative magnitude of transcellular and paracellular chloride transport and the details of luminal and basolateral chloride translocation steps.

Animals↗
PubMed2002

Chloride channels and hepatocellular function: prospects for molecular identification.

Hepatocytes possess chloride channels at the plasma membrane and in multiple intracellular compartments. These channels are required for cell volume regulation and acidification of intracellular organelles. Evidence also supports a role of chloride channels in modulation of apoptosis and cell growth. Swelling- and Ca(2+)-activated chloride channels have been identified in hepatocyte plasma membranes, and chloride channels have been observed in the membranes of lysosomes, endosomes, Golgi, endoplasmic reticulum, mitochondria, and the nucleus. This review summarizes the functions of these channels and discusses the specific channel molecules they may represent. Chloride channel molecules shown to be expressed in hepatocytes include members of the ClC channel family (ClC-2, ClC-3, ClC-5, and ClC-7), members of the newly identified CLIC family of intracellular chloride channels (CLIC-1 and CLIC-4), the mitochondrial voltage-dependent anion channel, and a newly identified intracellular channel, MCLC (Mid-1 related chloride channel). Current understanding does not include a molecular identification of most of the observed channel functions, but details of the molecular properties of these channel molecules should allow future identification and further understanding of chloride channel function in hepatocytes.

Animals↗
PubMed1981

Intracellular chloride activity in rabbit papillary muscle: effect of ouabain.

Intracellular chloride activity (aiCl) and membrane potential (Vm) were measured in rabbit papillary muscle under in vitro conditions. The cellular chloride concentration (Cli) was estimated from measurements of total water content, extracellular space, and total chloride concentration. The effects of therapeutic (10(-8) M) and toxic (10(-6) M) concentrations of ouabain on these parameters were tested. The chloride-sensitive microelectrodes were of the liquid-ion exchanger type. Selectivity for HCO-3 was taken into account in the calculation of aiCl. In 11 control experiments made with two different protocols aiCl was determined in subendocardial and in deeper cells. The mean membrane potentials were -78.7 and -78.0 mV and the mean cytoplasmic chloride activities were 17.5 and 17.7 mM, respectively. The chloride equilibrium potentials were -43.5 and -43.2 mV. These results indicated that chloride is not passively distributed in rabbit papillary muscle. Ouabain (10(-8) M) did not change Vm or aiCl. At a toxic concentration of ouabain, Vm fell to -68.0 mV in superficial cells and to -67.8 mV in deeper cells, but aiCl remained unchanged . These results suggested that under in vitro conditions intracellular chloride is distributed within more than one cellular compartment.

Animals↗
PubMed1986

Proton inhibition of chloride exchange: asynchrony of band 3 proton and anion transport sites?

The inhibition of chloride exchange at 0 degrees C by protons at the cytoplasmic and the extracellular surface of the band 3 protein of human erythrocytes was measured between pH 4.6 and 7.6. At constant external pH and chloride concentration, internal protons were a mixed inhibitor of chloride flux, with the apparent pK2 = 6.1 for protonation of the inward-facing empty transporter conformation and the apparent pK3 = 5.7 for protonation of the chloride-transporter complex. The activation of chloride exchange by external chloride was inhibited by internal protons, and internal protonation of the externally facing empty conformation had a pK1 = 6.1. External protons were also a mixed inhibitor of chloride exchange with the apparent pK1 = 5.0 for the empty outward-facing transporter conformation. Because of the pHo dependence of self-inhibition, the value of pK3 on the outside for chloride could not be accurately determined, but the apparent pK3 for protonation of the iodide-transporter complex on the extracellular surface was 4.9. The data support a mechanism with a single proton binding site that can alternatively have access to the cytoplasmic and extracellular solutions. It appears that this proton binding and transport site can be coupled to the single anion transport site for cotransport, but the two sites can be on opposite sides of the membrane at the same time and thus can be asynchronously transported by conformational changes of band 3.

Adult↗
PubMed1996

Monoclonal antibody against conductive chloride transport in pig ileal apical membrane vesicles.

Conductive chloride transport in the small intestine is an important factor controlling fluid movement from the blood to the lumen of the gut. Several proteins with potential conductive chloride ion channel activity are expressed in the enterocyte cell population. However, it is not clear whether one or more than one protein species is normally responsible for mediating conductive chloride transport. We have raised monoclonal antibodies that inhibit conductive chloride transport in apical membrane vesicles prepared from porcine ileal enterocytes. These monoclonal antibodies have been used to identify a unique protein involved with this conductive chloride transport. Here, we report that anti-chloride conductance monoclonal antibodies did not detect any antigen in Western blots of enterocyte apical membrane protein. Dot blotting and immunoprecipitation experiments indicated that the antigen recognized by these monoclonal antibodies was not the cystic fibrosis transmembrane conductance regulator. The antigen was localized to both villus and crypt regions of ileum on immunohistochemistry. A 90-kDa protein species was immunoprecipitated from a primary enterocyte cell line by these monoclonal antibodies. This 90-kDa protein may be a chloride ion channel or may play some regulatory role in conductive chloride transport in enterocyte apical membrane vesicles.

Animals↗
PubMed1977

Activity of chloride in absorptive cells of Amphiuma small intestine.

Double-barreled chloride-selective microelectrodes constructed by a new method have been used to determine intracellular chloride activity (aic1) in the absorptive cells of isolated, stripped proximal and distal segments of Amphiuma small intestine. Chloride was passively distributed across the mucosal membrane in fall and winter animals and aic1 is about 20 mM. In contrast summer animals actively accumulated chloride in both proximal and distal segments. Parallel measurements of intracellular chloride concentration (Cic1) reveal a very low apparent chloride activity coefficient (aic1/CiC1) indicating that all of the chloride is not free in the cytoplasm. The chloride activity in the bath immediately adjacent to the mucosa is higher than in the bulk solution.

Amphibians↗
PubMed1995

Osmolality-induced changes in aldosterone secretion involve a chloride-dependent process.

Alterations in extracellular osmolality have a powerful inverse effect on aldosterone secretion that is associated with sustained changes in cell volume. With dispersed bovine glomerulosa cells grown in primary culture, the effects of alterations in osmolality on cell volume measured by the distribution of [14C]urea and [3H]mannitol were determined in the presence and absence of chloride. In the presence of chloride, decreases in osmolality increased cell volume, whereas angiotensin II (< 4 x 10(-9) M) did not affect cell volume. When chloride was removed from the medium (replacing chloride with the impermeant methyl sulfate ion), cell volume decreased significantly, but basal aldosterone secretion was not altered. In the absence of chloride, the increases in cell volume, cytosolic calcium concentration, and aldosterone secretion induced by decreases in osmolality were significantly suppressed. The replacement of chloride with the methyl sulfate ion suppressed the increases in both cytosolic calcium concentration and aldosterone secretion induced by low (< 4 x 10(-9) M) but not high (4 x 10(-8) M) concentrations of angiotensin II. The results suggest that reductions in osmolality increase cell volume, partly by inducing an influx of chloride ions that contributes to the total net influx of water. Reductions in cell volume caused by an increase in osmolality or by replacing the chloride ion with the impermeant methyl sulfate ion may induce alterations in membrane stretch that may decrease the angiotensin II-induced increase in cytosolic calcium concentrations, which in turn suppresses aldosterone secretion.

Aldosterone↗
PubMed1999

Chloride cell subtypes in the gill epithelium of Japanese eel Anguilla japonica.

The purpose of the present study was to characterize chloride cell subtypes in the fish gill and to monitor the kinetic change of cell division in the gill epithelia during seawater adaptation. Employing a three-step Percoll gradient method, the gill chloride cells and nonchloride cell population were isolated. The isolated cells were studied using multiparameter flow cytometry, recording the changes in 1) cell size, 2) cellular granularity, and 3) cell autofluorescence. Two chloride cell subtypes were identified in the freshwater eels. Within 2-4 days after entering seawater, new subtypes of transitory chloride cell, with bigger cell size and more intense mitochondria autofluorescence, appeared. After full adaptation, two major seawater chloride cell subtypes were again discerned; their sizes were the largest and their mitochondria autofluorescence was the highest. In the second part of the experiment, cell cycle analysis demonstrated a progressive increase in the percentage of gill cells entering the DNA synthesis phase during seawater adaptation, where a small population of mitotic cells was identified in the nonchloride cell population but not in chloride cells. We hypothesize that the mitotic cells identified are stem cells, which will ultimately differentiate into seawater chloride cells. Our results confirm the existence of heterogeneity of chloride cells. Individual subtypes could be isolated in high purity for further studies to elucidate their respective function in mediating ion transport.

Anguilla↗
PubMed1978

Coupling between chloride absorption and base excretion in isolated skin of Rana esculenta.

The net excretory fluxes of base (HCO3- or OH-) and the unidirectional fluxes of chloride were measured and their relationship examined in isolated frog skin maintained in open- or short-circuit (OC and SC) conditions. When the mucosal solution was a 2 mM choline chloride solution and the serosal solution a Ringer solution buffered with a HCO3-/CO2 mixture, the rate of base excretion was -105 +/- 10 in OC and -60 +/- 7 neq h-1 cm-2 in SC. A highly significant correlation was observed between the influx of chloride and the excretion of base. As a function of external chloride both these parameters followed saturation kinetics, Vmax being obtained for a chloride concentration below 2 mM. The removal of chloride in the external solution was followed by a 70 or 100% inhibition of base excretion in OC and SC conditions, respectively. Chloride transport is dependent on the presence of a HCO3-/CO2 mixture in the internal or the external medium. This transport, as well as base excretion, is inhibited to a considerable extent by removal of HCO3-/CO2 or by acetazolamide (10(-3) M). This investigation characterizes a saturable transport system in which chloride absorption and base excretion are coupled.

Acetazolamide↗
PubMed1985

Stimulation of distal potassium secretion by low lumen chloride in the presence of barium.

Potassium secretion into the renal distal tubule is increased when chloride in the tubule fluid is replaced by another anion. The present experiments were done to determine whether this increment in transported potassium traverses a conductive pathway from cell to lumen. Transport rates of potassium, sodium, chloride, and fluid by the renal distal tubule of rats were examined in vivo by continuous microperfusion. The effects of substituting gluconate for chloride in the presence and absence of 5 mM barium in the perfusion fluid were determined. When gluconate replaced chloride in the perfusion solutions, potassium secretion increased (by 44%) without a significant change in transepithelial voltage. Barium in the lumen increased the magnitude of the lumen-negative transepithelial voltage (by 30%) and reduced potassium secretion (by 56%) by inhibiting conductive potassium movement. Barium also decreased both sodium (by 51%) and chloride (by 37%) absorption. Barium did not reduce the stimulation of potassium secretion caused by reducing lumen chloride concentration. Potassium secretion increased (by 77%) when lumen chloride was reduced in the presence of 5 mM barium. We interpret these results by postulating that a cotransport mechanism linking potassium and chloride is present in the luminal membrane of distal tubule cells, that this mechanism operates in parallel with a conductive transport pathway for potassium, and that the K-Cl cotransport mechanism is not inhibited by barium.

Animals↗
PubMed2000

In vivo role of CLC chloride channels in the kidney.

Chloride channels in the kidney are involved in important physiological functions such as cell volume regulation, acidification of intracellular vesicles, and transepithelial chloride transport. Among eight mammalian CLC chloride channels expressed in the kidney, three (CLC-K1, CLC-K2, and CLC-5) were identified to be related to kidney diseases in humans or mice. CLC-K1 mediates a transepithelial chloride transport in the thin ascending limb of Henle's loop and is essential for urinary concentrating mechanisms. CLC-K2 is a basolateral chloride channel in distal nephron segments and is necessary for chloride reabsorption. CLC-5 is a chloride channel in intracellular vesicles of proximal tubules and is involved in endocytosis. This review will cover the recent advances in research on the CLC chloride channels of the kidney with a special focus on the issues most necessary to understand their physiological roles in vivo, i.e., their intrarenal and cellular localization and their phenotypes of humans and mice that have their loss-of-function mutations.

Animals↗
PubMed1990

Luminal chloride modulates rat distal tubule bidirectional bicarbonate flux in vivo.

The effects of replacing luminal chloride with gluconate on distal tubule bicarbonate transport were studied in vivo in normally fed rats, overnight-fasted rats, and rats made mildly alkalotic by administration of desoxycorticosterone acetate (DOCA). In paired microperfusions of the same tubule with 0 or 55 mM Cl at 25 nl/min, net secretion of bicarbonate by distal tubules of fed rats was inhibited by chloride replacement. Zero chloride perfusion in DOCA rats also resulted in an inhibition of net bicarbonate secretion at 25 nl/min. In contrast, replacement of 45 mM chloride also perfused at 25 nl/min in fasted rats caused an increase in net bicarbonate reabsorption. To further characterize the effects of changes in luminal chloride, experiments were undertaken in fasted rats with 0, 45, and 100 mM chloride-containing solutions perfused at 8 and 25 nl/min. Perfusion with zero Cl resulted in net bicarbonate reabsorption at 8 nl/min that increased markedly with high flow, whereas bicarbonate reabsorption did not change significantly during perfusion at high flow with a 45-mM Cl perfusate. In marked contrast, perfusion with a 100-mM Cl solution resulted in only minimal bicarbonate reabsorption at 8 nl/min with significant secretion observed at high flow. Thus, chloride-free perfusates inhibit bicarbonate secretion and enhance bicarbonate reabsorption, while high chloride perfusates elicit net bicarbonate secretion in usually reabsorbing distal tubules.

Acid-Base Equilibrium↗
PubMed1996

Maturation of rabbit proximal convoluted tubule chloride permeability.

Chloride transport in the rabbit proximal convoluted tubule (PCT) has components of active, transcellular, and passive, paracellular transport. The preferential reabsorption of bicarbonate and organic solutes by the early proximal tubule leaves the luminal fluid with a higher chloride concentration than that in the peritubular capillaries. Previous studies have suggested that solute permeability of the paracellular pathway may be higher in the neonatal PCT and that the neonatal proximal tubule reabsorbs solutes by passive mechanisms to a greater extent than the adult segment. A higher chloride permeability would provide a mechanism for the greater rate of passive NaCl transport by the neonatal proximal tubule. The purpose of the present in vitro microperfusion study was to directly examine the chloride permeability of neonatal and adult PCT. Superficial and juxtamedullary, neonatal and adult PCT were perfused with a high chloride perfusate without organic solutes, simulating late proximal tubular fluid, at 20 degrees C, and bathed in a serum-like albumin solution. Chloride concentrations in the perfusate and the collected fluid were measured by electrometric titration. Neonatal juxtamedullary PCT chloride permeability (PCl) was significantly lower than adult juxtamedullary PCT PCl (0.15 +/- 0.25 x 10(-5) cm/s versus 5.23 +/- 0.57 x 10(-5) cm/s, p < 0.001). The PCl of neonatal superficial PCT was not different from that of adult superficial PCT (0.81 +/- 0.48 x 10(-5) cm/s versus 0.05 +/- 0.62 x 10(-5) cm/s). Thus, there is a maturational increase in juxtamedullary PCT PCl, whereas superficial PCT PCl remains very low. The passive diffusion of chloride in neonatal PCT is extremely low and is not a mechanism to explain a higher rate of passive NaCl transport in this segment.

Animals↗
PubMed1996

In vivo measurement of chloride and water secretion in the jejunum of cystic fibrosis patients.

In the present study, we have investigated the possible consequences of the chloride channel defect in the intestine of cystic fibrosis (CF) patients for electrolyte and water transport in the jejunum in vivo, using a multilumen, double occluding balloon catheter, and an Ag/AgCl intraluminal electrode. During a chloride-free perfusion, to optimize the sensitivity of our measurements, the transmural potential difference (PD) (lumen with reference to serosal side) was found to be significantly higher in the jejunum of CF patients (+8.0 +/- 2.1 mV; n = 5) than in healthy control subjects (-2.2 +/- 2.0 mV; n = 9). The chloride concentration measured in chloride-free jejunal perfusates of CF patients was significantly lower than in controls (10.9 +/- 2.3 and 41.4 +/- 8.2 mM, respectively). Possible differences in net chloride and water secretion did not reach statistical significance (chloride secretion controls: -2.1 +/- 0.9 mmol/10 cm/h; CF: -0.8 +/- 0.2 mmol/10 cm/h; water secretion controls: -0.8 +/- 2.5 mL/10 cm/h; CF: -11.7 +/- 8.9 mL/10 cm/h). In control subjects, intraluminally applied theophylline stimulated the secretion of water (delta 23.4 +/- 4.6 mL/10 cm/h) and chloride (delta 4.1 +/- 1.1 mmol/10 cm/h), but not in CF patients (respectively delta 3.6 +/- 3.3 mL/10 cm/h and delta 1.1 +/- 1.1 mmol/10 cm/h). In controls, theophylline caused a significant increase in lumen negativity (PD -10.2 +/- 2.6 mV), but no change could be seen in CF patient transmural PD. These observations provide in vivo evidence for a decreased chloride permeability in the jejunum in CF, resulting in a significant reduction in net electrolyte and water secretion in the presence, but not in the absence, of an intestinal secretagogue.

Adolescent↗
PubMed2003

Short-term transformation and long-term replacement of branchial chloride cells in killifish transferred from seawater to freshwater, revealed by morphofunctional observations and a newly established 'time-differential double fluorescent staining' technique.

Short- and long-term responses to direct transfer from seawater to freshwater were examined in gill chloride cells of killifish, which developed distinct freshwater- and seawater-type chloride cells in the respective environments. In a short-term response within 24 h after transfer, seawater-type chloride cells forming a pit structure on the apical surface were transformed into freshwater-type cells equipped with developed microvilli on the flat or projecting apical membrane, via the intermediate type. The transformation process was accompanied by the disappearance of apically located Cl- channel (cystic fibrosis transmembrane conductance regulator) and neighboring accessory cells. Chloride cell replacement was also examined as a long-term adaptation to freshwater transfer, using a newly established 'time-differential double fluorescent staining (TDS)' technique. In the TDS technique, in vivo labeling of chloride cells was performed on two separate days, using two distinguishable mitochondria-specific fluorescent probes. For 3 days after freshwater transfer, 14.7% of seawater-type cells were replaced with newly differentiated freshwater-type cells, whereas these ratios of chloride cell replacement were much lower (1.2% and 1.8%) in seawater- and freshwater-maintained groups, respectively. In consequence, following direct transfer of killifish from seawater to freshwater, seawater-type chloride cells were transformed morphologically and functionally into freshwater-type cells as a short-term response, followed by the promotion of chloride cell replacement as a long-term response.

Acclimatization↗
PubMed1992

Enhancing effect of sodium chloride on in vitro adsorption of paraquat onto activated carbon.

The enhancing effect of sodium chloride addition on the adsorption of paraquat onto activated carbon was discussed from the standpoints of equilibrium amount adsorbed and adsorption rate in vitro. The amount of paraquat adsorbed was increased by the addition of sodium chloride. The amount adsorbed with 0.1% addition was about five times greater than that in sodium chloride-free solution at an equilibrium concentration of 1 mg/L. The adsorption rate of paraquat onto activated carbon was also accelerated by sodium chloride addition. Kinetic constants in 0.1% and 0.9% sodium chloride solution were about 1.4 and 2.0 times greater, respectively, than that in sodium chloride-free solution. It was confirmed that paraquat removal by activated carbon was enhanced by sodium chloride addition. The reason was assumed to be the interrupted dissociation of paraquat in solution caused by sodium chloride addition.

Adsorption↗