Microbial release of 226Ra2+ from (Ba,Ra)SO4 sludges from uranium mine wastes

226Ra2+ is removed from uranium mine effluents by coprecipitation with BaSO4. (Ba,Ra)SO4 sludge samples from two Canadian mine sites were found to contain active heterotrophic populations of aerobic, anaerobic, denitrifying, and sulfate-reducing bacteria. Under laboratory conditions, sulfate reduction occurred in batch cultures when carbon sources such as acetate, glucose, glycollate, lactate, or pyruvate were added to samples of (Ba,Ra)SO4 sludge. No external sources of nitrogen or phosphate were required for this activity. Further studies with lactate supplementation showed that once the soluble SO4(2-) in the overlying water was depleted, Ba2+ and 226Ra2+ were dissolved from the (Ba,Ra)SO4 sludge, with the concurrent production of S2-. Levels of dissolved 226Ra2+ reached approximately 400 Bq/liter after 10 weeks of incubation. Results suggest that the ultimate disposal of these sludges must maintain conditions to minimize the activity of the indigenous sulfate-reducing bacteria to ensure that unacceptably high levels of 226Ra2+ are not released to the environment.     

Distribution of 226Ra body burden of workers in an underground uranium mine in India

Uranium mine workers are exposed to ore dust containing uranium and its daughter products during different mining operations. These radionuclides may pose inhalation hazards to workers during the course of their occupation. The most significant among these radionuclides is ²²⁶Ra. The measurement of radium body burden of uranium mine workers is important to assess their internal exposure. For this purpose, the radon-in-breath measurement technique has been used in the present paper. Workers at the Jaduguda mine, India, associated with different categories of mining operations were monitored between 2001 and 2007. The measurement results indicate that workers—depending on mining operation category—show ²²⁶Ra body burdens ranging from 0.15 to 2.85 kBq. The maximum body burden was found for workers associated with timbering operations, with an average ²²⁶Ra body burden of 0.85 ± 0.54 kBq. Overall, the average value observed for 800 workers was 0.76 ± 0.51 kBq, which gives rise to an average effective dose of 1.67 mSv per year for inhalation and 0.21 mSv per year for ingestion.     

Ba2+ ions inhibit the release of Ca2+ ions from rat liver mitochondria

The release of Ca2+ from respiring rat liver mitochondria following the addition of either ruthenium red or an uncoupler was measured by a Ca2+-selective electrode or by 45Ca2+ technique. Ba2+ ions are asymmetric inhibitors of both Ca2+ release processes. Ba2+ ions in a concentration of 75 microM inhibited the ruthenium red and the uncoupler induced Ca2+ release by 80% and 50%, respectively. For the inhibition, it was necessary that Ba2+ ions entered the matrix space: Ba2+ ions did not cause any inhibition of Ca2+ release if addition of either ruthenium red or the uncoupler preceded that of Ba2+. The time required for the development of the inhibition of the Ca2+ release and the time course of 140Ba2+ uptake ran in parallel. Ba2+ accumulation is mediated through the Ca2+ uniporter as 140Ba2+ uptake was competitively inhibited by extramitochondrial Ca2+ and prevented by ruthenium red. Due to the inhibition of the ruthenium red insensitive Ca2+ release, Ba2+ shifted the steady-state extramitochondrial Ca2+ concentration to a lower value. Ba2+ is potentially a useful tool to study mitochondrial Ca2+ transport.     

Ba2+ release from soda glass modifies single maxi K+ channel activity in patch clamp experiments.

Glasses used to fabricate patch pipettes may release components which affect ion channels (Cota, G., and C.M. Armstrong. 1988. Biophys. J. 53:107-109; Furman, R.E., and J.C. Tanaka. 1988. Biophys. J. 53:287-292; Rojas, L., and C. Zuazaga. 1988. Neurosci. Lett. 88:39-44). The gating properties of maxi K+ channels from Necturus gallbladder epithelium depend on whether borosilicate glass (BG) or blue tip hematocrit glass (SG) is used to construct the patch pipettes. The data are consistent with solubilization from SG of a component which exerts voltage-dependent, cytosolic-side specific block, closely resembling "slow block" by Ba2+ ions. Ringer's solution preincubated with SG, but not with BG, blocked inside-out maxi K+ channels when used as bathing solution. Mass spectrometry revealed that Ba2+ is released by the glass from fast and slow-release compartments (SG contains 3% wt/wt BaO), and is the only ion found in the solution at concentrations consistent with the observed channel block. Additionally, SG released O2-, Na+, Ca2+, and Mg2+, all to micromolar concentrations. These elements do not interfere with maxi K+ channels but they could in principle alter the properties of other ion channels. Thus, screening for channel-modifying substances released by the glass may be necessary for the adequate interpretation of patch-clamp results.     

Ba2+ stimulation of luteinizing-hormone release demonstrates two mechanisms of Ca2+ entry in gonadotrope cells.

Kinetic studies on gonadotropin-releasing-hormone (gonadoliberin, GnRH)-stimulated luteinizing-hormone (lutropin, LH) release in the cultured rat gonadotrope demonstrated a biphasic pattern of LH release. The first rapid phase of release was unaffected by the voltage-gated Ca2+-channel blockers methoxyverapamil (D600) and nifedipine [a dihydropyridine (DHP)], whereas the later second phase was partially inhibited by both drugs. These results suggested that the initial phase of LH release is independent of Ca2+ entry through dihydropyridine (DHP)-sensitive Ca2+ channels and might depend on entry of extracellular Ca2+ by another mechanism. These mechanisms were further studied by utilizing Ba2+ as a Ca2+ substitute. Ba2+, which freely permeates DHP-sensitive Ca2+ channels in the absence of GnRH, induced LH release which was sensitive to blockade by D600 and nifedipine. However, in the presence of the channel blockers, Ba2+-induced LH release could be elicited when GnRH was added to the system. This indicates that GnRH stimulates LH release by initially activating a DHP-insensitive Ca2+-entry mechanism and then a DHP-sensitive mechanism. The DHP-sensitive mechanism freely allows Ba2+ entry in the absence of GnRH-receptor occupancy, whereas the DHP-insensitive mechanism requires GnRH-receptor activation for Ba2+ entry.     

Green‐light emission through energy transfer from Ce3+ to Tb3+ ions in the Li2SO4–Al2(SO4)3 system

An energy transfer process from Ce³⁺ to Tb³⁺ ions was successfully achieved in a Li₂SO₄–Al₂(SO₄)₃ mixed‐sulphate system. A wet‐chemical synthesis was employed to prepare the Li₂SO₄–Al₂(SO₄)₃ system by doping Ce³⁺ and Tb³⁺ ions individually as well as collectively. The phases were identified using X‐ray diffraction studies. The as‐prepared samples were characterized by FT‐IR and photoluminescence measurements. Green‐light emission was exhibited by Ce³⁺, Tb³⁺ co‐doped Li₂SO₄–Al₂(SO₄)₃ system, thus, indicating its potential as a material for display devices or in the lamp industry.     

Interaction of internal Ba2+ with a cloned Ca(2+)-dependent K+ (hslo) channel from smooth muscle

We have studied potassium currents through a cloned Ca(2+)-dependent K+ channel (hslo) from human myometrium. Currents were recorded in inside- out macropatches from membranes of Xenopus laevis oocytes. In particular, the inactivation-like process that these channels show at high positive potentials was assessed in order to explore its molecular nature. This current inhibition conferred a bell shape to the current- voltage curves. The kinetic and voltage dependence of this process suggested the possibility of a Ba2+ block. There were the following similarities between the inactivation process observed at zero-added Ba2+ and the internal Ba2+ block of hslo channels: (a) in the steady state, the voltage dependence of the current inhibition observed at zero-added Ba2+ was the same as the voltage dependence of the Ba2+ block; (b) the time constant for recovery from current decay at zero- added Ba2+ was the same as the time constant for current recovery from Ba2+ blockade; and (c) current decay was largely suppressed in both cases by adding a Ba2+ chelator [(+)-18-crown-6-tetracarboxylic acid] to the internal solution. In our experimental conditions, we determined that the Kd for the complex chelator-Ba2+ is 1.6 x 10(-10) M. We conclude that the current decay observed at zero-added Ba2+ to the internal solution is due to contaminant Ba2+ present in our solutions (approximately 70 nM) and not to an intrinsic gating process. The Ba2+ blocking reaction in hslo channels is bimolecular. Ba2+ binds to a site (Kd = 0.36 +/- 0.05 mM at zero applied voltage) that senses 92 +/- 25% of the potential drop from the internal membrane surface.     

Drug-induced Ca2+ release from isolated sarcoplasmic reticulum. II. Releases involving a Ca2+-induced Ca2+ release channel

Calcium ions that have been preloaded into isolated sarcoplasmic reticulum subfractions in the presence of ATP and pyrophosphate may be released upon addition of a large number of diverse pharmacologic substances. We report here that not only caffeine, but also Ca2+ ions, thymol, quercetin, menthol, halothane, chloroform, 1-ethyl-2-methylbenzimidazole, ryanodine, tetraphenylboron, ketoconazole, miconazole, clotrimazole, W-7, doxorubicin, 5,5'-dithiobis-(2-nitrobenzoic acid), p-chloromercuribenzoic acid, and low concentrations of Ag+ induce Ca2+ release from such triadic sarcoplasmic reticulum. All these drugs induce increased undirectional Ca2+ efflux. We believe all these drug-induced Ca2+ releases are mediated by Ca2+ efflux through the same ion channel since these releases are all greatly attenuated when light sarcoplasmic reticulum is substituted for triads and are even more pronounced when transverse tubule-free terminal cisternae are substituted for triads, and all these forms of drug-induced Ca2+ release are inhibited by submicromolar concentrations of ruthenium red, and by submillimolar concentrations of tetracaine, 9-aminoacridine, and Ba2+, yet they are not affected by nifedipine even at a concentration of 50 microM.     

Drug-induced Ca2+ release from isolated sarcoplasmic reticulum. III. Block of Ca2+-induced Ca2+ release by organic polyamines

Calcium ions that have been preloaded into isolated SR subfractions in the presence of ATP and pyrophosphate may be released upon addition of a large number of diverse pharmacologic substances in a manner that is effectively blocked by ruthenium red and other organic polyamines. Effective blocking substances include certain antibiotics (neomycin, gentamicin, streptomycin, clindamycin, kanamycin, and tobramycin), naturally occurring polyamines (spermine and spermidine), and a number of basic polypeptides and proteins (polylysine, polyarginine, certain histones, and protamine). These agents have only one feature in common: the presence of several amino groups. Ruthenium red, neomycin, spermine, and protamine all appear to act by blocking SR Ca2+ channels since unidirectional 45Ca2+ efflux from the vesicles is strongly inhibited by these agents. Functions ascribable to the SR Ca2+ pump are largely unaffected by these agents. Since inositol 1,4,5-trisphosphate is ineffective at inducing Ca2+ release under these conditions, we conclude that these polyamines may directly block SR Ca2+ channels at very low concentrations by a mechanism unrelated to effects on inositol 1,4,5-trisphosphate production.     

Synthesis and photoluminescence properties of Eu3+‐activated Ba2Mg(PO4)2 phosphor

In this paper, we have reported the photoluminescence (PL) properties of the Ba₂Mg(PO₄)₂:Eu³⁺ phosphor synthesized using a wet chemical method. The preliminary scanning electron microscopy (SEM) investigation of the sample revealed irregular surface morphology with particle sizes in the 10–50 μm range. The strongest PL excitation peak was observed at 396 nm. The emission spectra indicated that this phosphor can be effectively excited by the 396 nm wavelength. Upon 396 nm excitation, the emission spectrum showed characteristics peaks located at 592 nm and 615 nm. These intense orange‐red emission peaks were obtained due to f→f transitions of Eu³⁺ ions. The emission peak at 592 nm is referred to as the magnetic dipole ⁵D₀→⁷F₁ transition and the emission peak at 615 nm corresponded to the electric dipole ⁵D₀→⁷F₂ transition of Eu³⁺. The Commission Internationale de l’Eclairage (CIE) coordinates of the Ba₂Mg(PO₄)₂:Eu³⁺ phosphor were found to be (0.586, 0.412) for wavelength 592 nm and (0.680, 0.319) for wavelength 615 nm situated at the edge of the CIE diagram, indicating high colour purity of phosphors. Due to the high emission intensity and a good excitation profile, Eu³⁺‐doped Ba₂Mg(PO₄)₂ phosphor may be a promising orange‐red phosphor candidate for solid‐state lighting applications.     

Luminescence characteristics of Na3Ca2(SO4)3F: Ce3+ fluoride material

A new Na₃Ca₂(SO₄)₃F: Ce³⁺ phosphor synthesized by a solid state diffusion method is reported. The photoluminescence study showed a single high intensity emission peak at 307 nm wavelength when excited by UV light of wavelength 278 nm. An unresolved peak of comparatively less intensity was also observed at 357 nm along with the main peak. The characteristic emission of dopant Ce in Na₃Ca₂(SO₄)₃F phosphor clearly indicated that it resides in the host lattice in trivalent form. The emission peak can be attributed to 5d → 4f transition of rare earth Ce³⁺. The prepared sample is also characterized for its thermoluminescence properties. The TL glow curve of prepared sample showed a single broad peak at 147°C. The trapping parameters are also evaluated by Chen's method. The values of trap depth (E) and frequency factor (s) were found to be 0.64 ± 0.002 eV and 1.43 × 10⁷ s^–1 respectively. The study of PL and TL along with evaluation of trapping parameters has been undertaken and discussed for the first time. Copyright © 2014 John Wiley & Sons, Ltd.     

Inositol (1,4,5)trisphosphate-promoted Ca2+ release from microsomal fractions of rat liver

Crude mitochondrial fractions containing a substantial amount of microsomes accumulate Ca2+ in the presence of ATP, ruthenium red and oligomycin. A proportion of this accumulated Ca2+ is released by the addition of low concentrations (ca. 1 microM) of inositol (1,4,5) trisphosphate . Under some conditions the release is transient, and evidence is presented which suggests that this is due to inhomogeneity in the vesicle population. (1,4,5)inositol trisphosphate -induced Ca2+ release can also be demonstrated, under appropriate experimental conditions, in a more purified microsomal fraction essentially free of mitochondria.     

Drug-induced Ca2+ release from isolated sarcoplasmic reticulum. I. Use of pyrophosphate to study caffeine-induced Ca2+ release

A demonstration is made of pyrophosphate's use as a precipitating anion in studies of Ca2+ release from isolated sarcoplasmic reticulum (SR). Not only does pyrophosphate speed up the rate at which Ca2+ can be preloaded into SR, but it also allows the accumulated Ca2+ to be released in response to agents such as caffeine. Because so much Ca2+ can be preloaded into SR with pyrophosphate present, more experiments can be performed with a given amount of SR material, and even rapid Ca2+ release rates (greater than 1 mumol/mg X min) are maintained for many seconds. These rates can easily be quantified using conventional spectrophotometric and isotopic methods, without the need for expensive rapid mixing equipment. Caffeine-induced Ca2+ release is exhibited by triadic and terminal cisterna SR subfractions but not by light SR. Caffeine specifically increases the rate of unidirectional 45Ca2+ efflux. This increased efflux is blocked by ruthenium red at submicromolar concentrations and by tetracaine, 9-aminoacridine, or Ba2+ at submillimolar concentrations.     

Inhibitors of Ca2+ release from the isolated sarcoplasmic reticulum. II. The effects of dantrolene on Ca2+ release induced by caffeine, Ca2+ and depolarization

The effects of dantrolene, which is a known muscle relaxant, on Ca2+ release from the isolated sarcoplasmic reticulum induced by several different methods [1) addition of caffeine, (2) Ca2+ jump, and (3) membrane-depolarization produced by choline chloride replacement of potassium gluconate) were investigated. Dantrolene inhibited caffeine-induced Ca2+ release with C1/2 = 2.5 microM, whereas there was no effect on Ca2+ release induced by a Ca2+ jump. The amount of Ca2+ released by depolarization was reduced if Ca2+ release was triggered in an earlier phase of the steady state of Ca2+ uptake (time elapsed between the addition of ATP and the triggering of Ca2+ release, tATP less than 4 min); while, if triggered in a latter phase (tATP greater than 4 min) dantrolene enhanced depolarization-induced Ca2+ release. C1/2 for the inhibition and that for enhancement of depolarization-induced Ca2+ release were 1.0 and 0.3 microM, respectively. These results suggest that dantrolene affects several different steps of the mechanism by which Ca2+ release is triggered. The sarcoplasmic reticulum and T-tubule membrane fractions had 7.9 nmol dantrolene-binding sites/mg (Kassoc = 1.0 X 10(5) M-1) and 21.0 nmol/mg (Kassoc = 1.1 X 10(5) M-1), respectively. The time-course of dantrolene binding to sarcoplasmic reticulum was monophasic, while that to T-tubules was biphasic.     

Photoluminescence in K3Ca2(SO4)3Cl‐doped Eu3+ phosphor

In this article we report Eu³⁺ luminescence in novel K₃Ca₂(SO₄)₃Cl phosphors prepared by wet chemical methods. The Eu³⁺ emission was observed at 594 nm and 615 nm, keeping the excitation wavelength constant at 396 nm nearer to light‐emitting diode excitation, Furthermore, phosphors were characterized by X‐ray diffraction for the confirmation of crystallinity. The variation of the photoluminescence intensity with impurity concentration has also been discussed. Thus, prominent emission in the red region makes prepared phosphors more applicable for white light‐emitting diodes. Copyright © 2013 John Wiley & Sons, Ltd.     

Active, Irreversible Accumulation of Extreme Levels of H(2)SO(4) in the Brown Alga, Desmarestia

The brown algae Desmarestia ligulata var. ligulata (Lightf.) Lamour., and D. viridis (Mull.) Lamour., accumulate H₂SO₄ until their average internal pH is 0.5 to 0.8. A related species, D. aculeata (L.) Lamour., does not accumulate acid. The H₂SO₄ accumulation is accompanied by a reduction in the K⁺ and Cl⁻ content, presumedly to maintain osmotic balance. Measurements of the membrane potential and H⁺ and SO₄²⁻ concentrations indicate that both ions are accumulated in the vacuole against their electrochemical potential gradients.

The internal pH remains constant in all three species over the growing season, despite striking changes in the algal morphology. The pH is not affected by periods of darkness of up to 34 hours. Sulfate accumulated in the vacuoles appears to be trapped there since incubation of D. ligulata for up to 10 days in sulfate-free medium resulted in little loss of either vacuolar sulfate or H⁺. Although the uptake of H₂SO₄ into the vacuole must require energy, the maintenance of the vacuolar H₂SO₄ may be due to the impermeability of the tonoplast, with little necessity for continued expenditure of energy.

     

Flux of SO(2) into Leaf Cells and Cellular Acidification by SO(2)

A comparison of fluxes of SO₂ from the atmosphere into leaves with fluxes across biomembranes revealed that, apart from the cuticle, the main barrier to SO₂ entry into leaves are the stomates. SO₂ fluxes into leaves can be calculated with an accuracy sufficient for many purposes on the assumption that the intracellular SO₂ concentration is zero. SO₂ entering green leaf cells is trapped in the cytoplasm. In the light, the products formed in its reaction with water are processed particularly in the chloroplasts. Flux of SO₂ to the acidic central vacuole of leaf cells is insignificant. Intracellular acidification of barley mesophyll protoplasts by SO₂ was measured by the uptake of ¹⁴C-labeled 5,5-dimethyl-oxazolidine-2,4-dione. The measured acidification was similar to the acidification calculated from known buffer capacities and the rate of SO₂ influx when the H⁺/SO₂ ratio was assumed to be 2. A comparison of photosynthesis inhibition by SO₂ with calculated acidification revealed different mechanisms of inhibition at low and at high concentrations of SO₂. At very low concentrations, inhibition by SO₂ was even smaller than expected from calculated acidification. The data suggest that, if acidification cannot be compensated by pH-stabilizing cellular mechanisms, it is a main factor of SO₂ toxicity at low SO₂ levels. At high levels of SO₂, anion toxicity and/or radical formation during oxidation of SO₂ to sulfate may play a large role in inhibition.     

Anion-mediated Fe3+ release mechanism in ovotransferrin C-lobe: a structurally identified SO4(2-) binding site and its implications for the kinetic pathway

The differential properties of anion-mediated Fe(3+) release between the N- and C-lobes of transferrins have been a focus in transferrin biochemistry. The structural and kinetic characteristics for isolated lobe have, however, been documented with the N-lobe only. Here we demonstrate for the first time the quantitative Fe(3+) release kinetics and the anion-binding structure for the isolated C-lobe of ovotransferrin. In the presence of pyrophosphate, sulfate, and nitrilotriacetate anions, the C-lobe released Fe(3+) with a decelerated rate in a single exponential progress curve, and the observed first order rate constants displayed a hyperbolic profile as a function of the anion concentration. The profile was consistent with a newly derived single-pathway Fe(3+) release model in which the holo form is converted depending on the anion concentration into a "mixed ligand" intermediate that releases Fe(3+). The apo C-lobe was crystallized in ammonium sulfate solution, and the structure determined at 2.3 A resolution demonstrated the existence of a single bound SO(4)(2-) in the interdomain cleft, which interacts directly with Thr(461)-OG1, Tyr(431)-OH, and His(592)-NE2 and indirectly with Tyr(524)-OH. The latter three groups are Fe(3+)-coordinating ligands, strongly suggesting the facilitated Fe(3+) release upon the anion occupation at this site. The SO(4)(2-) binding structure supported the single-pathway kinetic model.