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At least 37 records · Page 2Linked to original sources
PubMed1997

Heavy-metal toxicity in an insect cell line. Effects of cadmium chloride, mercuric chloride and methylmercuric chloride on cell viability and proliferation in Aedes albopictus cells.

We evaluated the toxicity of CdCl2, HgCl2, and MeHgCl on the C6/36 cell line of Aedes albopictus. This cell line proved to be a suitable tool for studying heavy-metal toxicity in insect cells. Since data on heavy-metal toxicity in invertebrate cell cultures are almost nonexistent, our results are discussed in relation to in vivo invertebrate and in vitro vertebrate studies. Viability and proliferation were assessed by dye exclusion and DNA quantification, respectively. Viability tests were carried out with and without 5% fetal calf serum in the medium. The three metal species decreased viability to different extents (MeHgCl > HgCl2 > CdCl2), and fetal calf serum had a protective effect. In serum-deprived cultures, LD50 values were 140.20, 2.51, and 2.08 mumol/L for CdCl2, HgCl2, and MeHgCl, respectively. For cultures with fetal calf serum, LD50 values were 149.71, 12.01, and 5.47 mumol/L, respectively. The viability curve for CdCl2 under serum-free conditions suggests the induction of a cell defense system. The three metal species also inhibited cell proliferation (MeHgCl > CdCl2 > HgCl2). The IC50 values were 1.75, 18.36, and 0.96 mumol/L for CdCl2, HgCl2, and MeHgCl, respectively. In summary, low MeHgCl concentrations caused both cell death and inhibition of cell proliferation; HgCl2 primarily disrupted the plasma membrane, whereas CdCl2 primarily inhibited cell proliferation.

Aedes↗
PubMed1983

Effect of chloride on renin and blood pressure responses to sodium chloride.

Both the inhibition of renin release by sodium chloride and salt-sensitive hypertension have been attributed to sodium. We evaluated the contribution of chloride to these responses to sodium chloride. In the Sprague-Dawley rat, acute and chronic administration of sodium salts other than sodium chloride failed to suppress plasma renin activity, whereas renin was inhibited by both sodium chloride and by selective chloride (without sodium) loading. Plasma renin activity was stimulated by selective chloride depletion. Similarly, in humans, plasma renin activity was suppressed by sodium chloride but not by sodium bicarbonate infusion. In a preliminary study in the Dahl salt-sensitive rat, in contrast to sodium chloride loading, sodium bicarbonate loading failed to produce hypertension. Thus, both the renin and possibly the blood pressure responses to sodium chloride are dependent on chloride.

Adult↗
PubMed1985

Active chloride transport in rabbit thick ascending limb of Henle's loop and elasmobranch rectal gland: chloride fluxes in isolated plasma membranes.

To investigate directly whether a sodium-potassium-chloride cotransport system is operating in the mammalian thick ascending limb of Henle's loop (TALH) and in the elasmobranch rectal gland, plasma membrane vesicles were prepared from TALH cells isolated from rabbit kidney outer medulla and from rectal glands of Squalus acanthias, and chloride uptake was measured by a rapid filtration technique. Chloride uptake into TALH vesicles in the presence of a 25 mM Na2SO4, 25 mM K2SO4 gradient reached 70% of equilibrium at 2.5 min. In the presence of both sodium and potassium, the 15 s chloride uptake was inhibited 35% by 1 mM bumetanide. When either sodium or potassium was removed from the incubation medium, chloride uptake decreased to the level observed in the presence of 1 mM bumetanide, 0.5 mM SITS had no effect on chloride uptake by the plasma membrane vesicles. This sodium and potassium dependent, bumetanide sensitive chloride uptake was also observed under tracer exchange conditions. Chloride uptake into rectal gland plasma membrane vesicles in the presence of a 50 mM Na2SO4, 50 mM K2SO4 gradient reached 80% of equilibrium at 2.5 min. 1 mM bumetanide inhibited the 15 s uptake of chloride by 34% and removal of either sodium or potassium from the incubation medium reduced chloride uptake to the level observed in the presence of bumetanide under both gradient and tracer exchange conditions. These studies provide additional support for the hypothesis that a sodium-potassium-chloride cotransport system is operating in these epithelia.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1994

Electrodiffusive movements of chloride ion in sodium-free solution: a possible calcium activated chloride conductance in cultured heart cells.

OBJECTIVE: The aim was to demonstrate that removal of extracellular sodium (Na+o), a manoeuvre known to increase intracellular calcium (Cai2+), can activate a chloride ion conductance in cultured embryonic chick heart cells. METHODS: Intracellular chloride activity (aiCl) and membrane potentials (Em) were simultaneously measured using chloride selective and 3 M KCl filled microelectrodes. RESULTS: In Na+o-free and K+o-free solutions, a frusemide (0.3 mM) resistant decrease in aiCl of 10 mM was recorded within 10 min, along with a 5 mV hyperpolarisation, and the calculated chloride equilibrium potential (ECl) followed the change of Em, suggesting a possibly enhanced chloride conductance. When cells were exposed to Na+o-free solution, the decrease of aiCl by approximately 10 mM was associated with an initial depolarisation, followed by a hyperpolarisation to approximately -60 mV (more negative than ECl). Subsequent removal of K+o depolarised Em to -39 mV (approximately ECl), and no further loss of aiCl occurred. Restoration of K+o caused a hyperpolarisation of Em (more negative than ECl) and a continuing decline of aiCl. Prevention of K+o induced hyperpolarisation by addition of 1 mM Ba2+ stopped the decline of aiCl (Em approximately ECl), suggesting that following Na+o removal, alteration of the driving force for chloride led to a chloride efflux via an enhanced chloride conductance. When Em depolarised to -50 mV after 3 min exposure to 0.1 mM ouabain, removal of [Cl-]o caused a further depolarisation and readdition of [Cl-]o induced an 18 mV hyperpolarisation. This chloride induced hyperpolarisation was blocked by removal of [Ca2+]o (+1 mM EGTA). CONCLUSIONS: The increase in chloride conductance observed under conditions that are known to raise Ca2+i supports the presence of a Ca2+i activated chloride conductance in cultured chick heart cells.

Animals↗
PubMedDate not supplied

Chloride determination in foods with ion-selective electrode after isolation as hydrogen chloride.

This report describes a sample preparation method in which chloride is isolated as hydrogen chloride from food samples prior to analysis with the chloride ion-selective electrode. Chloride analyses of selected foods with this method agreed with chloride values reported in food composition tables. Chloride analysis with the present procedure also agreed with the certified value for the chloride content of the National Bureau of Standards (NBS) Standard Reference Material, Nonfat Milk Powder. Reliability of the chloride isolation procedure was evident by the complete recovery of chloride added to food samples and a narrow range of 95% confidence limits calculated for each set of analyses. The usefulness of the chloride ion-selective electrode to determine chloride in foods is greatly enhanced by this procedure because matrix interference by other sample components is removed prior to analysis.

Chlorides↗
PubMed1983

Sodium-chloride transport in the medullary thick ascending limb of Henle's loop: evidence for a sodium-chloride cotransport system in plasma membrane vesicles.

Sodium transport mechanisms were investigated in plasma membrane vesicles prepared from the medullary thick ascending limb of Henle's loop (TALH) of rabbit kidney. The uptake of 22Na into the plasma membrane vesicles was investigated by a rapid filtration technique. Sodium uptake was greatest in the presence of chloride; it was reduced when chloride was replaced by nitrate, gluconate or sulfate. The stimulation of sodium uptake by chloride was seen in the presence of a chloride gradient directed into the vesicle and when the vesicles were equilibrated with NaCl, KCl plus valinomycin so that no chemical or electrical gradients existed across the vesicle (tracer exchange experiments). Furosemide decreased sodium uptake into the vesicles in a dose-dependent manner only in the presence of chloride, with a Ki of around 5 X 10(-6) M. Amiloride, at 2 mM, had no effect on the chloride-dependent sodium uptake. Similarly, potassium removal had no effect on the chloride-dependent sodium uptake and furosemide was an effective inhibitor of sodium uptake in a potassium-free medium. The results show the presence of a furosemide-sensitive sodium-chloride cotransport system in the plasma membranes of the medullary TALH. There is no evidence for a Na+/H+ exchange mechanism or a Na+ -K+ -Cl- cotransport system. The sodium-chloride cotransport system would effect the uphill transport of chloride against its electrochemical potential gradient at the luminal membrane of the cell.

Anions↗
PubMed1978

Relation between chloride exchange diffusion and a conductive chloride pathway across the isolated skin of the toad (Bufo bufo).

Substitution of chloride in the outside bathing medium of the toad skin with bromide, iodide, nitrate and sulphate leads to a reduction in the apparent exchange diffusion of chloride across this tissue, and also to a reduction of the chloride current recorded during hyperpolarization. A series of inhibitors (thiocyanate, furosemide, phloretin, and acetazolamide) also affects chloride exchange diffusion, hyperpolarization current as well as chloride influx during hyperpolarization. Although in some cases, effects on the short circuit current were also observed none of the effects on chloride transport systems could be explained as secondary effects due to a primary interaction with the sodium transport mechanisms. A correlation was found between the clamping current recorded during hyperpolarization and the efflux of chloride under short circuit conditions with chloride Ringer's on both sides. On the basis of these findings, and the results reported in the previous paper (Hviid Larsen and Kristensen 1977) it is considered probable that the membrane molecules responsible to chloride exchange diffusion under short circuit conditions, are rearranged under the influence of a hyperpolarizing clamping voltage, thereby forming channels allowing charge transferring transport of chloride.

Acetazolamide↗
PubMed2000

Reversal of meconium inhibition of pulmonary surfactant by ferric chloride, copper chloride, and acetic acid.

Meconium inhibits pulmonary surfactant function. We investigated the in vitro effect of meconium on three different commercial surfactants. The dynamic surface properties of these surfactants were evaluated at the concentration of 5 mg/ml with a pulsating bubble system. The inhibitory effect of 2.75 mg/ml meconium was significantly less on Alveofact than on Curosurf and Survanta. Ferric chloride and copper chloride completely reversed the inhibitory effect of meconium. Meconium also prevented effective spreading of surfactant in a Wilhelmy balance system, and this inhibitory effect was counteracted by addition of ferric chloride. Image analysis of Curosurf demonstrated that meconium reduced the total number of microbubbles in 15 light-microscopic fields (4.35 mm(2)) from 1,748 +/- 481 to 180 +/- 166. Ferric chloride restored the number of microbubbles. Addition of ferric chloride or copper chloride to surfactant/meconium lowers pH, and pH adjustment by acetic acid also reversed the inhibitory effect of meconium. Together with the fact that the iron-chelator deferoxamine did not attenuate the effect of ferric chloride this suggests that the observed contrainhibition is caused by lowering of pH, and that meconium inhibition of surfactant is pH-dependent. Lowering pH from 6.2 to 5-5.5 abolished the inhibitory effects of meconium on surfactant. Inhibition of 2.5 mg/ml of Curosurf with plasma could also be reversed by increasing amounts of ferric chloride. We conclude that the inhibitory effect of meconium on surfactant in vitro can be abolished by addition of ferric chloride, copper chloride, or acetic acid.

Acetic Acid↗
PubMed1992

Inhibitory effect of calcium chloride on gastric carcinogenesis in rats after treatment with N-methyl-N'-nitro-N-nitrosoguanidine and sodium chloride.

The effects of calcium chloride on glandular stomach carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and sodium chloride were investigated in male outbred Wistar rats. Animals were given MNNG solution (100 p.p.m.) as drinking water and simultaneously fed a diet supplemented with 5% sodium chloride for 8 weeks. Matched negative controls received neither MNNG nor sodium chloride. Rats were then fed basal diet and given calcium chloride solution (1 or 0.2%) or tap water for the following 52 weeks. The incidences and multiplicities of preneoplastic hyperplasias in the glandular stomachs of rats given MNNG/sodium chloride followed by 1 and 0.2% calcium chloride were significantly lower than those in rats given MNNG/sodium chloride alone. The inhibitory effects of calcium were exerted in a dose-dependent manner. Calcium treatment also showed a tendency to inhibit the development of gastric adenocarcinomas although this was not statistically significant. Rats without carcinogen treatment had neither carcinomas nor preneoplastic hyperplasias in the glandular stomach. Calcium intake also significantly reduced the levels of malondialdehyde, a measure of lipid peroxidation, in the gastric mucosa and urine, the former in a dose-dependent manner. Thus, calcium chloride exerted inhibitory effects when given during the post-initiation phase of two-stage glandular stomach carcinogenesis in rats.

Animals↗
PubMed1986

Enhancement of fluoride retention by low dietary chloride without manifestation of chloride deficiency in the rat.

Weanling male albino rats were fed a purified diet containing 10 ppm fluoride as sodium fluoride and 0.02, 0.04, 0.06, 0.08, or 0.10% chloride as sodium chloride for 6 wk. Food intake was unaffected by the level of dietary chloride. Rats fed diets containing either 0.02 or 0.04% chloride had significantly higher fluoride retention and skeletal uptake of fluoride than did rats fed higher chloride levels. Diets, however, had to contain 0.04% chloride or more to support normal weight gain, femur ash weight and plasma chloride concentration. The ability to enhance fluoride content of bone on a low chloride diet without undesirable effects of chloride deficiency may have important implications, since fluoride is thought to play a role in strengthening the mineral apatite structure of bone.

Animal Nutritional Physiological Phenomena↗
PubMed1991

Studies on the role(s) of cerebrospinal fluid osmolality and chloride ion in the centrally mediated pressor responses of sodium chloride.

These studies were designed to investigate whether the centrally mediated pressor effects of hypertonic sodium chloride (NaCl) solutions are triggered in response to changes in the cerebrospinal fluid (CSF) osmolality and whether the chloride ion plays a role in these effects. In Inactin anesthetized, vagotomized rats, alterations in the arterial pressure to cerebroventricular administration (i.c.v.) of various concentrations of NaCl, sodium nitrate (NaNO3), glycerol, creatinine, lithium chloride (LiCl), lithium nitrate (LiNO3) and choline chloride were evaluated. The pressor effects of NaCl were significantly greater than those produced by either glycerol, creatinine and/or NaNO3 solutions. Central effects of NaCl were identical to that of LiCl; likewise, NaNO3 and LiNO3 produced essentially similar increases in the blood pressure. In other words, the two chloride salts produced significantly greater increases in the arterial pressure than the nitrate salts. Choline chloride also produced significant increases in the blood pressure both before and after pretreatment with hemicholinum (i.c.v.). In a separate series of experiments, pretreatment of rats with a vasopressin antagonist (i.v.), significantly attenuated the pressor effects of NaCl, NaNO3 and that of choline chloride whereas after autonomic ganglionic blockade with chlorisondamine, pressor responses of only NaCl, but not those of NaNO3 or choline chloride were significantly inhibited. These data indicate that elevation of either Na+ or Cl- in the CSF facilitates vasopressin secretion and that Na+ and Cl- ions function synergistically in the central nervous system (C.N.S.) to enhance sympathetic activity. The present studies demonstrate that the circumventricular structures in the C.N.S. that participate in the regulation of blood pressure are more responsive to changes in concentrations of Na+ and Cl- rather than to net changes in the CSF osmolality. The data further suggest that the chloride ion contributes to the central pressor effects of NaCl and may play a role in the pathophysiology of salt-dependent hypertension.

Angiotensin Receptor Antagonists↗
PubMed2000

Active intestinal chloride secretion in human carriers of cystic fibrosis mutations: an evaluation of the hypothesis that heterozygotes have subnormal active intestinal chloride secretion.

To explain the very high frequency of cystic fibrosis (CF) mutations in most populations of European descent, it has been proposed that CF heterozygotes have a survival advantage when infected with Vibrio cholerae or Escherichia coli, the toxins of which induce diarrhea by stimulation of active intestinal chloride secretion. Two assumptions underlie this hypothesis: (1) chloride conductance by the CF transmembrane conductance regulator (CFTR) is the rate-limiting step for active intestinal chloride secretion at all levels of expression, from approximately zero in patients with CF to normal levels in people who are not carriers of a mutation; and (2) heterozygotes have smaller amounts of functional intestinal CFTR than do people who are not carriers, and heterozygotes therefore secrete less chloride when exposed to secretagogues. The authors used an intestinal perfusion technique to measure in vivo basal and prostaglandin-stimulated jejunal chloride secretion in normal subjects, CF heterozygotes, and patients with CF. Patients with CF had essentially no active chloride secretion in the basal state, and secretion was not stimulated by a prostaglandin analogue. However, CF heterozygotes secreted chloride at the same rate as did people without a CF mutation. If heterozygotes are assumed to have less-than-normal intestinal CFTR function, these results mean that CFTR expression is not rate limiting for active chloride secretion in heterozygotes. The results do not support the theory that the very high frequency of CF mutations is due to a survival advantage that is conferred on heterozygotes who contract diarrheal illnesses mediated by intestinal hypersecretion of chloride.

Adolescent↗
PubMed1977

Mechanism of active chloride secretion by shark rectal gland: role of Na-K-ATPase in chloride transport.

The isolated rectal gland of Squalus acanthias was stimulated to secrete chloride against an electrical and a chemical gradient when perfused in vitro by theophylline and/or dibutyryl cyclic AMP. Chloride secretion was depressed by ouabain which inhibits Na-K-ATPase. Thiocyanate and furosemide also inhibited chloride secretion but ethoxzolamide, a carbonic anhydrase inhibitor, did not. Chloride transport was highly dependent on sodium concentration in the perfusate. The intracellular concentration of chloride averaged 70-80 meq/liter in intact glands, exceeding the level expected at electrochemical equilibrium and suggesting active transport of chloride into the cell. These features suggest a tentative hypothesis for chloride secretion by the rectal gland in which the uphill transport of chloride into the cytoplasm is coupled through a membrane carrier to the downhill movement of sodium along its electrochemical gradient. The latter is maintained by the Na-K-ATPase pump while chloride is extruded into the duct by electrical forces.

Adenosine Triphosphatases↗
PubMed2003

Abnormal passive chloride absorption in cystic fibrosis jejunum functionally opposes the classic chloride secretory defect.

Due to genetic defects in apical membrane chloride channels, the cystic fibrosis (CF) intestine does not secrete chloride normally. Depressed chloride secretion leaves CF intestinal absorptive processes unopposed, which results in net fluid hyperabsorption, dehydration of intestinal contents, and a propensity to inspissated intestinal obstruction. This theory is based primarily on in vitro studies of jejunal mucosa. To determine if CF patients actually hyperabsorb fluid in vivo, we measured electrolyte and water absorption during steady-state perfusion of the jejunum. As expected, chloride secretion was abnormally low in CF, but surprisingly, there was no net hyperabsorption of sodium or water during perfusion of a balanced electrolyte solution. This suggested that fluid absorption processes are reduced in CF jejunum, and further studies revealed that this was due to a marked depression of passive chloride absorption. Although Na+-glucose cotransport was normal in the CF jejunum, absence of passive chloride absorption completely blocked glucose-stimulated net sodium absorption and reduced glucose-stimulated water absorption 66%. This chloride absorptive abnormality acts in physiological opposition to the classic chloride secretory defect in the CF intestine. By increasing the fluidity of intraluminal contents, absence of passive chloride absorption may reduce the incidence and severity of intestinal disease in patients with CF.

Adult↗