Factors affecting the permeability of isolated fat-cells from the rat to [42K]potassium and [36Cl]chloride ions

1. The effluxes of (42)K(+) and (36)Cl(-) from isolated fat-cells from the rat were studied under a variety of conditions known to affect the metabolism of the cells. 2. (42)K(+) efflux from isolated fat cells was increased in a Na(+)-free-high-K(+) medium and decreased in a K(+)-free medium. The existence of K(+) exchange diffusion across the fat-cell membrane is suggested. 3. (36)Cl(-) efflux from isolated fat-cells was decreased when the Cl(-) component of the wash medium was replaced by acetate. The basal (36)Cl(-) efflux is suggested to be partly by Cl(-) exchange diffusion and partly in company with a univalent cation. 4. A variety of lipolytic stimuli, adrenaline, adrenocorticotrophic hormone, N-6,O-2'-dibutyryladenosine cyclic 3':5'-monophosphate and theophylline, increased (42)K(+) efflux from isolated fat-cells. The adrenaline stimulation was biphasic; an initial, rapid and transient increase in (42)K(+) loss from the fat-cells was followed by a slower, more prolonged, increase in (42)K(+) efflux. The initial phase was inhibited by phentolamine but not by propranolol. 5. Insulin increased (42)K(+) efflux only after preincubation with the cells.     

Efflux of chloride from lactating rat mammary tissue slices

1. The efflux of chloride (using 36Cl) from lactating rat mammary tissue slices has been investigated. 2. Chloride efflux was found to be temperature dependent; lowering the temperature of the incubation medium reduced the fractional efflux. 3. The stilbene derivatives DIDS was without effect on the fractional release of Cl when studied at 20 degrees C. However, DIDS was found to attenuate the increase in efflux found upon transferring the tissue from a medium maintained at 4 degrees C to one at 20 degrees C. 4. The loop-diuretic furosemide, also reduced the temperature-sensitive portion of Cl efflux. 5. Chloride efflux was transiently increased when tissue slices were transferred from a medium containing gluconate as the principal anion to one containing Cl. 6. The results appear to confirm that mammary Cl transport is mediated via anion exchange and via (Na + K + Cl) cotransport.     

Anion/anion exchange in human neutrophils

Of the total one-way chloride fluxes (approximately 1.4 meq/liter cell water X min) in steady state human polymorphonuclear leukocytes bathed in 148 mM Cl media, approximately 70% behaves as self-exchange mediated by a nonselective anion carrier that is not inhibited by stilbene disulfonates. Five properties of this carrier-mediated exchange were investigated: substrate saturation is seen with respect to 36Cl influx as a function of the external Cl concentration [for normal-Cl cells, the apparent Km(Cl) is approximately 22 mM when Cl replaces para-amino- hippurate (PAH) and approximately 5 mM when Cl replaces glucuronate], and with respect to 36Cl efflux as a function of the concentration of internal Cl replacing PAH [apparent Km(Cl) congruent to 35 mM for cells bathed in 148 mM Cl]; there is trans stimulation of 36Cl influx by internal Cl (replacing PAH) with an apparent Km(Cl) congruent to 35 mM, and of 36Cl efflux by external Cl with an apparent Km(Cl) congruent to 22 mM (Cl replacing PAH) or approximately 5 mM (Cl replacing glucuronate); there is substrate competition between Cl and PAH, but the carrier appears devoid of affinity for glucuronate; influxes and effluxes mediated by the carrier are subject to competitive inhibition by extracellular alpha-cyano-4-hydroxycinnamate (CHC), with an apparent Ki congruent to 9 mM in Cl medium or approximately 1 mM in PAH medium (transport of the inhibitor itself is very slow); and internal Cl and external Cl or PAH undergo 1:1 countertransport, which is CHC sensitive. A simple equilibrium-competition model is proposed that accounts for all the extracellular ligand interactions presented for normal-Cl cells. Least-squares values of the carrier's true Michaelis constants for extracellular Cl, PAH, and CHC are 5.03 +/- 0.83, 50.3 +/- 14.9, and 0.29 +/- 0.09 mM, respectively.     

Contribution of mucosal chloride to chloride in toad bladder epithelial cells

Summary Epithelial cells were scraped from the bladders of toads of the speciesBufo marinus obtained from the Dominican Republic. These epithelial cells exchanged their chloride virtually completely with³⁶Cl in the medium within 60 min. Of this chloride, about 93% came from the serosal medium. The approximately 20 mmole/kg dry wt of chloride which equilibrates with³⁶Cl in the mucosal medium was still present when choline replaced sodium in the medium in the presence of amiloride (10^–4 M) and was almost all readily removed by rapid washing of the mucosal surface immediately prior to analysis. These observations suggest that little chloride of mucosal origin is truly intracellular. This conclusion is supported by the fact that after vasopressin the increased cellular chloride was not of mucosal origin.     

Stimulation of Na+/Mg2+ antiport in rat erythrocytes by intracellular Cl-

Mg(2+) efflux from rat erythrocytes was measured in NaCl, NaNO(3), NaSCN and Na gluconate medium. Substitution of extracellular and intracellular Cl(-) with the permeant anions NO(3)(-) and SCN(-) reduced Mg(2+) efflux via Na(+)/Mg(2+) antiport. After substitution of extracellular Cl(-) with the non-permeant anion gluconate, Mg(2+) efflux was not significantly reduced. In Na gluconate medium, an influence of the changed membrane potential and intracellular pH on Mg(2+) efflux could be excluded. The results indicate the existence of Cl(-)-independent Na(+)/Mg(2+) antiport and of Na(+)/Mg(2+) antiport stimulated by intracellular Cl(-). Intracellular Cl(-), as determined by means of (36)Cl(-), was found to stimulate Na(+)/Mg(2+) antiport through a cooperative effect according to a sigmoidal kinetics. The Hill coefficient for intracellular Cl(-) amounted to 1.4-1.8, indicating that two intracellular Cl(-) may be simultaneously active. With respect to specificity, Cl(-) was most effective, followed by Br(-), J(-), and F(-). Stimulation of Na(+)/Mg(2+) antiport by intracellular Cl(-) together with intracellular Mg(2+) may play a role during deoxygenation of erythrocytes and in essential hypertension.     

Volume-induced increase of anion permeability in human lymphocytes

Peripheral blood mononuclear cells (PBM) readjust their volumes after swelling in hypotonic media. This regulatory volume decrease (RVD) is associated with a loss of cellular K+ and is thought to be promoted by an increased permeability to this ion. In contrast, no change in volume was observed when K+ permeability of PBM in isotonic media was increased to comparable or higher levels using valinomycin. Moreover, valinomycin-induced 86Rb+ loss in K+-free medium was considerably slower than in K+-rich medium. These results suggest that anion conductance limits net salt loss in isotonic media. Direct measurements of relative conductance confirmed that in volume-static cells, anion conductance is lower than that of K+. In volume-regulating cells depolarization occurred presumably as a result of increased anion conductance. Accordingly, the efflux of 36Cl from PBM was markedly increased by hypotonic stress. Since both membrane potential and intracellular 36Cl concentration are reduced in hypotonically swollen cells, the increased efflux is probably due to a change in Cl- permeability. Anions and cations seem to move independently through the volume-induced pathways: the initial rate of 86Rb uptake in swollen cells was not affected by replacement of external Cl- by SO=4; conversely, 36Cl fluxes were unaffected by substitution of K+ by Na+. The data indicate that anion conductance is rate-determining in salt and water loss from PBM. An increase in anion conductance is suggested to be the critical step of RVD of human PBM.     

A cystic fibrosis phenotype in cells cultured from sweat gland secretory coil. Altered kinetics of 36Cl efflux

As a step toward understanding the metabolic consequences of the cystic fibrosis (CF) mutation, we have examined the kinetics of 36Cl efflux in cells cultured from sweat glands, a tissue that is affected in the disease. Epithelial cells, derived from the secretory coil of sweat glands of CF and control individuals, were cultured in serum-free medium, and primary cultures used for efflux experiments. Cell layers were equilibrated with Na36Cl in 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid-buffered balanced salt solution for 45 min at 37 degrees C, washed in 0.25 M sucrose, and incubated in nonradioactive buffer for measurement of 36Cl efflux. Efflux from CF and control cells followed biphasic kinetics and was described by the equation Y = Ae-kat + Be-kbt. All efflux was inhibited at 6 degrees C. The fast component of efflux, Ae-kat, of both control and CF cells was inhibited by the anion channel blockers 4,4'-diisothiocyanato-2,2'-stilbene disulfonic acid, 9-anthracene carboxylate, and diphenylamine 2-carboxylate, implicating release through chloride channels. At 23 degrees C, the kinetics of 36Cl efflux from CF and control cells were indistinguishable, but efflux from control cells could be accelerated by cAMP analogs and isoproterenol. At 37 degrees C, 36Cl efflux was more rapid from control cells than from CF cells, but could not be stimulated further by beta-adrenergic agents. In both cases, the increased rate of efflux was due to a severalfold increase in the A parameter of the fast component. These differential responses constitute a "CF phenotype" of secretory sweat gland cells in culture that may be useful for further investigation of the metabolic defect in cystic fibrosis.     

The Hiroshima thermal-neutron discrepancy for 36Cl at large distances. Part I: New 36Cl measurements in granite samples exposed to A-bomb neutrons

The long-lived radioisotope (36)Cl (half-life: 301,000 years) was measured in granite samples exposed to A-bomb neutrons at distances from 94 to 1,591 m from the hypocenter in Hiroshima, by means of accelerator mass spectrometry (AMS). Measured (36)Cl/Cl ratios decrease from 1.6 x 10(-10) close to the hypocenter to about 1-2 x 10(-13), at a distance of 1,300 m from the hypocenter. At this distance and beyond the measured (36)Cl/Cl ratios do not change significantly and scatter around values of 1-2 x 10(-13). These findings suggest that the (36)Cl had been predominantly produced by thermalized neutrons from the A-bomb via neutron capture on stable (35)Cl, at distances from the hypocenter smaller than about 1,200 m. At larger distances, however, confounding processes induced by cosmic rays or neutrons from the decay of uranium and thorium become important. This hypothesis is theoretically and experimentally supported in a consecutive paper. The results are compared to calculations that are based on the most recent dosimetry system DS02. Close to the hypocenter, measured (36)Cl/Cl ratios are lower than those calculated, while they are significantly higher at large distances from the hypocenter. If the contribution of the cosmic rays and of the neutrons from the decay of uranium and thorium in the sample was subtracted, however, no significant deviation from the DS02 calculations was observed, at those distances. Thus, the Hiroshima neutron discrepancy reported in the literature for (36)Cl for samples from large distances from the hypocenter, i.e., higher measured (36)Cl/Cl ratios than predicted by the previous dosimetry system DS86, was not confirmed.     

Hypotonic shock activated Cl- and K+ pathways in human fibroblasts.

The exposure of human fibroblasts to hypotonic medium (200 mosmolal) evoked the activation of both 36Cl- influx and efflux, which were insensitive to inhibitors of the anion exchanger and of the anion/cation cotransport, and conversely were inhibited by the Cl(-)-channel blocker 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB). 36Cl- efflux was linked to a parallel efflux of 86Rb+; thus conductive K+ and Cl- pathways are activated during volume regulation in human fibroblasts. This conclusion is supported by evidence that, in hypotonic medium, 36Cl- influx and 86Rb+ efflux were both enhanced by depolarization of the plasma membrane. Depletion of the intracellular K+ content, obtained by preincubation with the ionophore gramicidin in Na(+)-free medium, had no effect on Cl- efflux in hypotonic medium. This result has been interpreted as evidence for independent activation of K+ and Cl- pathways. It is also concluded that the anion permeability is the rate-limiting factor in the response of human fibroblasts to hypotonic stress.     

Carrier-Mediated Transport of Chloride Across the Blood-Brain Barrier

36Cl concentrations in each of eight brain regions and in cisternal cerebrospinal fluid (CSF) were determined 30 min after the intravenous injection of 36Cl in dialyzed-nephrectomized rats with plasma Cl concentrations between 14 and 120 mumol X ml-1. CSF 36Cl exceeded 36Cl concentrations in brain extracellular fluid. The calculated blood-to-brain transfer constants for Cl, kCl, ranged from 1.8 X 10(-5) S-1 at the parietal cortex to 3.8 X 10(-5) S-1 at the thalamus-hypothalamus. kCl fell by 42-62% when mean plasma [Cl] was elevated from 16 to 114 mumol X ml-1. Brain uptake of [14C]mannitol or of 22Na was independent of plasma [Cl], but 22Na influx into CSF fell when plasma [Cl] was reduced. Cl flux into brain and CSF could be represented by Michaelis-Menten saturation kinetics, where, for the parietal cortex, Km = 43 mumol X ml-1 and Vmax = 2.5 X 10(-3) mumol X S-1 X g-1, and for CSF Km = 68 mumol X ml-1. At least 80% of 36Cl influx into the parietal cortex was calculated to occur at the cerebrovascular endothelium, whereas the remainder was derived from tracer that first entered CSF. The CSF contribution was greater at brain regions adjacent to cerebral ventricles. The results show that Cl transport at the cerebrovascular endothelium as well as at the choroid plexus epithelium is a saturable concentration-dependent process, and that the CSF is a significant intermediate pathway for Cl passage from blood to brain.     

Volatile compounds from the mycelium of the mushroom Agaricus bisporus

The pattern of volatiles from the mycelium of two commercial strains of Agaricus bisporus, grown in axenic culture on a semi-synthetic medium, was found to be broadly similar to that of the volatiles identified from sporophores. Tetrachloro-1,4-dimethoxybenzene, a known secondary metabolite of several Basidiomycetes, was found in the mycelium though not in the sporophores. [³⁶Cl]Tetrachloro-1,4-dimethoxybenzene was obtained when sodium [¹³Cl]chloride was added to the medium.     

36Cl measurements in Hiroshima granite samples as part of an international intercomparison study. Results from the Munich group

Within the effort to resolve the so-called Hiroshima neutron discrepancy, an international intercomparison study has been carried out on granite samples from Hiroshima, with participating institutions from Japan, the US, and Germany. (36)Cl and (152)Eu produced in these samples by thermal neutrons from the A-bomb explosion were assessed independently by means of different techniques. At the Maier-Leibnitz-Laboratory near Munich, Germany, (36)Cl concentrations were measured by accelerator mass spectrometry. Measured (36)Cl/Cl ratios ranged from 1,670 x 10(-13) (at a distance of 146 m from the hypocenter) to 2.2 x 10(-13) (at a distance of 1,163 m from the hypocenter). One granite sample not exposed to A-bomb neutrons was measured as a control, and a (36)Cl/Cl ratio of 2.6 x 10(-13) was obtained. On average, our experimental results are 20-30% lower than those provided by model calculations based on the dosimetry system DS86. The results presented here do not support previous assessments of (36)Cl, (60)Co, and (152)Eu which had suggested much larger thermal neutron fluences than those calculated on the basis of DS86 for distances from the hypocenter of more than 1,000 m.     

Stoichiometry of a half-turnover of band 3, the chloride transport protein of human erythrocytes

The kinetics of human red blood cell Cl transport have been studied under nonequilibrium conditions to determine whether or not an outward Cl gradient can recruit the transport protein from an inward-facing to an outward-facing configuration. Three kinds of evidence are consistent with this outward recruitment. First, the initial net Cl efflux into a Cl-free phosphate medium is independent of the intracellular Cl concentration in the range 20-170 mM. Second, an outward Cl gradient strongly enhances the inhibitory potency of DNDS (4,4'-dinitro-2,2'-stilbene disulfonate), which suggests that DNDS binds primarily to outward-facing states. Finally, we have estimated the number of Cl ions transported during the putative outward recruitment. Resealed red cell ghosts containing only 70 muM 36Cl were resuspended at 0 degrees C in a Cl-free, HCO3-free Na2SO4 medium. In the first 10 s, or approximately 10(6) Cl ions per ghost, followed by a much slower further loss of Cl. The rapid loss of 10(6) Cl ions per ghost, which is abolished by pretreatment with DIDS (4,4'-diisothiocyano-2,2'-stilbene disulfonate), appears to represent the Cl that is transported during the first half-turnover of the transport cycle. These data are strong evidence that the influx and efflux events in the catalytic cycle for anion transport do not take place simultaneously, and that the stoichiometry of the transport cycle is close to one pair of anions exchanged per band 3 monomer.     

ATP-driven,Na(+)-independent inward Cl- pumping in neuroblastoma cells

In immature neurones, the steady-state intracellular Cl- concentration [Cl-](i) is generally higher than expected for passive distribution, and this is believed to be due to Na(+)-K(+)-2Cl(-) co-transport. Here, we show that N2a neuroblastoma cells, incubated in HEPES-buffered NaCl medium maintain a [Cl-](i) around 60 mm, two- to threefold higher than expected for passive distribution at a membrane potential of - 49 mV. When the cells were transferred to a Cl(-) -free medium, [Cl-](i) decreased quickly (t(1/2) < 5 min), suggesting a high Cl- permeability. When the intracellular ATP concentration was reduced to less than 1 mm by metabolic inhibitors, the initial rate of (36) Cl- uptake was strongly inhibited (60-65%) while steady-state [Cl-](i) decreased to 24 mm, close to the value predicted from the Nernst equilibrium. Moreover, after reduction of [ATP](i) and [Cl-](i) by rotenone, the subsequent addition of glucose led to a reaccumulation of Cl-, in parallel with ATP recovery. Internal bicarbonate did not affect Cl- pumping, suggesting that Cl-/HCO(3)(-) exchange does not significantly contribute to active transport. Likewise, Na(+) -K(+) -2Cl(-) co-transport also appeared to play a minor role: although mRNA for the NKCC1 form of the co-transporter was detected in N2a cells, neither the initial rate of (36)Cl- uptake nor steady-state [Cl-](i) were appreciably decreased by 10 microm bumetanide or replacement of external Na(+) by choline. These results suggest that a highly active ATP-dependent mechanism, distinct from Na(+) -K(+) -2Cl(-) co-transport, is responsible for most of the inward Cl- pumping in N2a cells.     

Actions of avermectin B1a on the gamma-aminobutyric acidA receptor and chloride channels in rat brain

The interaction of avermectin B1a (AVM) with the gamma-aminobutyric acid (GABA) receptor of rat brain was studied using radioactive ligand binding and tracer ion flux assays. Avermectin potentiated the binding of [3H]flunitrazepam and inhibited the binding of both [3H]muscimol and [35S]t-butylbicyclophosphorothionate to the GABAA receptor. Inhibition of muscimol binding by AVM suggested competitive displacement. Two kinds of 36chloride (Cl) flux were studied. The 36Cl efflux from preloaded microsacs was potentiated by AVM and was highly inhibited by the Cl-channel blocker 4,4'-diisothiocyano-2,2'-stilbenedisulfonic acid (DIDS). However, it was not potentiated by GABA nor was it sensitive to the convulsants picrotoxin or bicuculline. On the other hand, 36Cl-influx measurement in a different microsac preparation of rat brain was very sensitive to GABA and other GABA-ergic drugs. Avermectin induced 36Cl influx into these microsacs in a dose-dependent manner, but to only 35% of the maximal influx induced by GABA. The AVM-induced 36Cl influx was totally blocked by bicuculline. It is suggested that AVM opens the GABAA-receptor Cl channel by binding to the GABA recognition site and acting as a partial receptor agonist, and also opens a voltage-dependent Cl channel which is totally insensitive to GABA but is very sensitive to DIDS.     

Cerebrovascular Permeability Coefficients to Sodium, Potassium, and Chloride

CSF and regional brain concentrations of 42K, 22Na, 36Cl, and [14C]mannitol were determined 3-45 min after intravenous injection of the tracers in pentobarbital-anesthetized rats. Rapid influx of 36Cl and 22Na into ventricular CSF immediately established concentration gradients from CSF to brain extracellular fluid. The CSF contribution to brain uptake of tracers was greatest in periventricular brain regions, where brain 36Cl concentrations were up to ninefold higher than concentrations in regions distant from ventricular CSF. Acetazolamide (20 mg kg-1 i.p.), an inhibitor of CSF formation, decreased 36Cl uptake into CSF and into periventricular brain regions but not into frontal cortex. 36Cl uptake into brain was unidirectional for 10 min after intravenous injection, and, during that period, diffusion from ventricular CSF did not contribute to uptake in the frontal cortex. Therefore, cerebrovascular permeability coefficients could be calculated from tracer concentrations in frontal cortex at 10 min and equaled, in cm s-1, 13.5 X 10(-7) for 42K, 1.4 X 10(-7) for 22Na, 0.9 X 10(-7) for 36Cl, and 1.5 X 10(-7) for [14C]mannitol. The low cerebrovascular permeabilities to K, Na, and Cl, comparable to those of some cell membranes, and the permselectivity (K much greater than Na greater than Cl) suggest that a significant fraction of ion transport across cerebral capillaries is transcellular, i.e., across the endothelial cell membrane.     

Species selection for phytoremediation of 36Cl/35Cl using angiosperm phylogeny and inter-taxa differences in uptake

High concentrations of 35Cl and the radioisotope 36Cl (produced naturally by cosmic radiation and anthropogenically by U fission and the use of neutron sources) can be problematic in soil, but are potentially amenable to phytoremediation if appropriate plants can be found. Here, results are reported that might aid the selection of plants with unusually high or low uptake of 36Cl A residual maximum likelihood analysis was used to estimate, from 13 experiments, relative 36Cl uptake by 106 species across the angiosperm phylogeny. Nested analysis of variance, coded using a recent angiosperm phylogeny, showed that there were significant inter-species differences in 36Cl uptake and that species behavior was not independent; but linked through theirphylogeny. Eudicots had significantly higher 36Cl uptake than Monocots and related clades and, in particular the Orders Caryophyllales, Apiales, and Cucurbitales had high uptake while the Poales, Lillales, Brassicales, and Fabales had low uptake. Overall, 35% of the inter-taxa variation in 36Cl was attributed to the taxonomic ranks of Order and above, a significant phylogenetic effect compared with other elements for which similar analyses have been published. The implications of these findings for selecting plants for phytoremediation of soil contaminated with 35/36Cl are discussed.     

Transfer of Cl from herbage into tissues and milk products of dairy cattle and pigs

Cl-36 is an important component of nuclear waste. The concentrations of stable chlorine (Cl) in pig and cow tissues were measured to provide information which can be used to parameterize models of ³⁶Cl transfer into agricultural animals. The concentration of stable Cl in cows’ milk was 1.0 ± 0.2 g L⁻¹, in cow muscle it was 0.7 ± 0.2 g kg⁻¹ wet mass (wm) and in pig muscle 0.4 ± 0.1 g kg⁻¹ wm. The concentration of stable Cl in cow and pig liver was 0.9 ± 0.3 g kg⁻¹ wm, which was about two-fold higher than that in the kidney and lung. Due to homeostatic control, stable Cl concentrations in animal tissues are not related to the amount ingested daily in herbage at intake rates in the normal physiological range of up to 188 g day⁻¹ for cows and up to 40 g day⁻¹ for pigs. Therefore, the commonly used transfer coefficient is not suitable for use in quantifying the transfer of ³⁶Cl to milk and meat. Since the metabolism of stable Cl and ³⁶Cl in an animal’s body is identical, the average equilibrium ratios of ³⁶Cl to stable Cl in the daily ration (³⁶Cl (g kg⁻¹)/Cl (g kg⁻¹)) and animal tissues will be the same. We therefore conclude that the average equilibrium Cl isotopic ratio in the dietary daily intake should be used to predict the contamination of meat and milk with ³⁶Cl.     

Contrast in chloride exclusion between two grapevine genotypes and its variation in their hybrid progeny

Potted grapevines of 140 Ruggeri (Vitis berlandieri × Vitis rupestris), a good Cl(-) excluder, and K 51-40 (Vitis champinii × Vitis riparia 'Gloire'), a poor Cl(-) excluder, and of a family obtained by crossing the two genotypes, were used to examine the inheritance of Cl(-) exclusion. Rooted leaves were then used to further investigate the mechanism for Cl(-) exclusion in 140 Ruggeri. In both a potting mix trial (plants watered with 50 mM Cl(-)) and a solution culture trial (plants grown in 25 mM Cl(-)), the variation in Cl(-) accumulation was continuous, indicating multiple rather than single gene control for Cl(-) exclusion between hybrids within the family. Upper limits of 42% and 35% of the phenotypic variation in Cl(-) concentration could be attributed to heritable sources in the potting mix and solution culture trials, respectively. Chloride transport in roots of rooted leaves of both genotypes appeared to be via the symplastic pathway, since addition of 8-hydroxy-1,3,6-pyrenetrisulphonic acid (PTS), an apoplastic tracer, revealed no obvious PTS fluorescence in the laminae of either genotype, despite significant accumulation of Cl(-) in laminae of K 51-40 during the PTS uptake period. There was no significant difference in either unidirectional (36)Cl(-) flux (10 min) or (36)Cl(-) uptake (3 h) into roots of rooted leaves exposed to 5, 10, or 25 mM Cl(-). However, the percentage of (36)Cl(-) transported to the lamina (3 h) was significantly lower in 140 Ruggeri than in K 51-40, supporting reduced Cl(-) loading into xylem and implicating the root stele in the Cl(-) exclusion mechanism.     

The Hiroshima thermal-neutron discrepancy for 36Cl at large distances. Part II: Natural in situ production as a source

For Hiroshima, a large discrepancy between calculated and measured thermal-neutron fluences had been reported in the past, for distances to the epicenter larger than about 1,000 m. To be more specific, measured (36)Cl concentrations in environmental samples from Hiroshima were too large at these distances, and the ratio of measured to calculated values reached about 70, at a distance of 1,800 m. In an attempt to identify other sources that might also produce (36)Cl in Hiroshima samples, the role of cosmic rays and of neutrons from natural terrestrial sources was investigated. Four reaction mechanisms were taken into account: spallation reactions of the nucleonic (hadronic) component of the cosmic rays on potassium (K) and calcium (Ca) in the sample material, particle emission after nuclear capture of negative muons by K and Ca, reactions of fast-muon induced electromagnetic, and hadronic showers with K and Ca, and neutron capture reactions with (35)Cl in the sample where the neutrons originate from the above three reaction mechanisms and from uranium and thorium decay. These mechanisms are physically described and mathematically quantified. It is shown that among those parameters important for the production of (36)Cl in granite, the chemical composition of the sample, the depth in the quarry where the sample had initially been taken, and the erosion rate at the site of the quarry are most important. Based on these physical, chemical, and geological parameters, (36)Cl concentrations were calculated for different types of granite that are typical for the Hiroshima area. In samples that were of these granite types and that had not been exposed to atomic bomb(A-bomb) neutrons, the (36)Cl concentration was also determined experimentally by means of accelerator mass spectrometry, and good agreement was found with the calculated values. The (36)Cl signal due to natural in situ production was also calculated in granite samples that had been exposed to A-bomb neutrons at distances up to 1,500 m from the hypocenter. It is demonstrated that, for granite samples from Hiroshima exposed to A-bomb neutrons beyond distances of about 1,300 m from the hypocenter, the (36)Cl signal is dominated by natural in situ production.