Anion permeability of the olfactory receptive membrane.

The ionic mechanism of the electropositive olfactory receptor potential was studied in the bullfrog and the swamp frog. The positive receptor potential strikingly decreased in amplitude in chloride-free solution. When the olfactory epithelium was immersed in high-KCl-Ringer's solution and then in Cl-free, high-K solution, the polarity of the positive potential could be reversed. This is supposed to be due to the exit of the increased internal chloride ion. From the above two experiments it is concluded that the positive olfactory receptor potential depends primarily upon the influx of the chloride ion through the olfactory receptive membrane. Some contribution by potassium and possibly other ions may occur. The ability of other anions to substitute for chloride was examined. It was found that only Br-, F-, and HCO2- could penetrate the olfactory receptive membrane. The sieve hypothesis in the inhibitory post-synaptic membrane (Coombs, Eccles, and Fatt, 1955) is not applicable to the olfactory receptive membrane on the basis of the size of hydrated ions, but it may be applicable on the basis of the sizes of naked ions.

The effect of selected aromatic bromine derivatives on the activity of glutathione peroxidase and transferase.

OBJECTIVES: Glutathione (GSH) is an important element of antioxidative barrier. Its biological function consists in eliminating oxygen free radicals. It also acts as a co-substrate in numerous enzymatic reactions catalyzed by glutathione peroxidase (GPx) and glutathione S-transferase (GST). In our study we attempted to assess the effect of hexabromobenzene (HBB) and its metabolites on the level of GSH and related enzymes, GPx and GST. MATERIALS AND METHODS: The experiments were performed on female Wistar rats. The investigated compounds (HBB, 1,2,4,5-tetraBB, 1,2,4- and 1,3,5-triBB) were administered intragastrically in three different doses (HBB: 15, 75, and 375 mg/kg; 1,2,4,5-tetraBB and 1,2,4-triBB: 8, 40, and 200 mg/kg; 1,3,5-triBB: 12, 60, and 300 mg/kg) for 7, 14, 21 or 28 days. GSH level and activity of GST and GPx were determined in the obtained material. RESULTS: The highest activity of GPx and GSTwas observed after a 7-fold administration of all investigated compounds. Prolonged time of exposure caused the return to the control values. CONCLUSIONS: The study revealed that repeated exposure to aromatic bromine derivatives increases GPx and GST activity only in the initial phase of the experiment.

Effect of long-term administration of arsenic (III) and bromine with and without selenium and iodine supplementation on the element level in the thyroid of rat.

The aim of this study was to evaluate the influence of arsenic and bromine exposure with or without iodine and selenium supplementation on the element level in the thyroid of rats. Four major groups of Wistar female rats were fed with respective diets: group A - standard diet, group B - iodine rich diet (10 mg I/kg food), group C - selenium rich diet (1 mg Se/kg) and group D - iodine and selenium rich diet (as in group B and C). Each group was divided into four subgroups per 7 animals each receiving either NaAsO(2) ip (6.5 mg.kg(-1) twice a week for two weeks and 3.25 mg.kg(-1) for six weeks) or KBr in drinking water (58.8 mg.l(-1)) for 8 weeks or combined administration of both substances. Remaining subgroup served as controls. After 8 weeks thyroid glands were analyzed by ICP-MS for As, Br, Se, and I content. The exposition of rat to arsenic or bromine causes the accumulation of these elements in the thyroid gland ( approximately 18 ppm of As, approximately 90 ppm of Br) and significantly affects iodine and selenium concentration in the thyroid. In iodine and/or selenium supplemented rats the bromine intake into the thyroid was lowered to approximately 50% of the level in unsupplemented animals. Also selenium thyroid level elevated due to KBr administration was lowered by iodine supplementation in the diet. The accumulation of arsenic in the thyroid was not influenced by selenium or iodine supplementation; however, As(III) administration increased iodine thyroid level and suppressed selenium thyroid level in selenium or iodine supplemented group of animals.

[Rationale for treating patients with hypertension and atherosclerosis of the lower extremities with iodine-bromine baths containing molecular iodine].

Higher therapeutic efficacy of iodine-bromine baths in conversion of iodine from an ionic form (standard iodine-bromine baths) into a molecular one is registered. This is explained by a 23.8 times increase in precipitation and a 4-times increase in iodine penetration into the body when it is molecular. A more effective function of the cardiovascular system, a stronger corrective effect on lipid metabolism, microcirculation in the absence of changes in a secretory function of the thyroid were registered.

An improved bromide assay for the estimation of extracellular water volume by capillary gas chromatography.

A sensitive bromide determination has been developed that consists of the following steps: isolation (purification) of bromide; oxidation of bromide to bromine with potassium permanganate and subsequent reaction with acetone, to give the volatile bromoacetone; quantification of bromoacetone by capillary gas chromatography. The method can also be used with small sample volumes appropriate for paediatric applications. Thermodynamic arguments are used to calculate the equilibria involved. The accuracy and reproducibility of the method have been determined. Finally, the bromide space of six volunteers was determined and the clearance of the bromide by the kidneys was investigated.

Biological monitoring of workers' exposure to bromine.

The use of serum bromine concentration (SeBr) as a measure of exposure was examined in an occupational cohort. Associations with work site, department type, chemical handling, and occupation, as proxy measures of exposure, were studied. SeBr was associated with all of these measures. SeBr was also associated with various demographic characteristics (age, country of origin, and education) in men. In women, there was no association between SeBr and age, country of origin, or education. The use of SeBr as a measure of exposure is discussed. The conclusion is that the exposure to bromine can be assessed by regular monitoring of SeBr.

Biological half-life of bromine in the rat thyroid.

The biological half-life of bromine in the rat thyroid was determined by measuring the radioactivity of thyroids of animals which continuously received 82Br labelled bromide in their food. The value of this half-life (110 h) is practically the same as the biological half-life of iodine. The rate of establishing the I/Br concentration ratio in the thyroid depends on the biological half-life of bromine. The mechanism of this process depends on the state of iodine supply. When the supply is sufficient, the iodine concentration in the thyroid remains constant, while during iodine deficiency the iodine atoms are replaced by atoms of bromine.

In vitro analysis of bromine chemical burns with use of full-thickness human skin.

Parameters of bromine injury were studied in vitro with the use of full-thickness human skin (HS) specimens--discards from various surgical procedures. The morphology of in vitro-treated HS resembled that of in vivo-injured skin. The damage was pronounced in the epidermis (destruction of the stratum corneum, and extensive vacuolation of keratinocytes) and the dermis (collagen coagulation), depending on the bromine concentration, exposure time, and application method. A decreased viability of epidermal cells, assayed by dye exclusion, was observed as well. Permeation parameters of bromine via abdominal HS were determined by quantitating bromine concentration in the donor and receiving compartments. The amount of bromine that permeated HS was inversely related to the concentration gradient applied. This in vitro study suggests that prompt treatment and early medical intervention may be required for successful healing of both severe and mild cases of bromine injuries.

Effects of thyroparathyroidectomy on the distribution of bromine and iodine in rat tissues.

The concentrations of iodine (I) and bromine (Br) were measured by inductively coupled plasma mass spectrometry in the plasma, kidney, heart, liver, and brain of control and thyroparathyroidectomized (TPTX) rats without and with an additional intake of either NaI or NaBr, 0.5 and 5 mumol/kg/d, respectively, for 21 d. In all groups, the highest concentrations of I and Br were found in the plasma. TPTX did not modify the concentrations of I in tissues, but slightly increased Br in plasma (+33%) and kidney (+24%). The additional intake of I with the drink induced an increase of I concentrations in the tissues tested (from 54 to 191%), except brain, both in control and TPTX rats. This additional intake of I also increased Br levels in the plasma of control (+24%) and TPTX rats (+53%). The additional intake of Br with the drink induced an increase of Br levels in all the tested tissues, brain included (from 85 to 284%). The augmentation was higher in the tissues, particularly brain, of TPTX rats than of controls. The increase of Br in brain after an additional intake contrasts with the absence of increase of I given in the same conditions. This difference between I and Br probably results from the smaller radius of Br ion in comparison with I ion radius. In conclusion, TPTX did not modify the distribution of I in the tested tissues, but slightly increased the concentrations of Br in plasma and kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Interaction of bromine with iodine in the rat thyroid gland at enhanced bromide intake.

In experiments with rats, we have found that at enhanced intake of bromide, bromine does not replace chlorine in the thyroid; it replaces iodine. Under our experimental conditions, more than one-third of the iodine content in the thyroid was replaced by bromine. In the thyroid, bromine probably remained in the form of bromide and, in proportional to its increased concentration, the production of iodinated thyronines decreased, with the sum of the iodine and bromine concentrations being constant at the value of 20.51 +/- 1.16 mumol/g dry wt of the thyroid. In contrast to other organs, the biological behavior of bromine in the thyroid is not similar to the biological behavior of chlorine but resembles more that of iodine.

Effect of automobile exhaust on the distribution of trace elements and its modulation following Fe, Cu, and Zn supplementation.

The effect of automobile exhaust on the distribution of trace elements with special reference to Pb and its modulation following Cu, Zn, and Fe supplementation, in mouse organs, has been studied using Energy Dispersive X-ray Fluorescence technique. Seven elements, namely K, Fe, Cu, Zn, Br, Rb, and Pb, were detected in all the organs. The maximum concentration of Pb was found in lungs followed by that in liver and kidney. The effect of automobile exhaust was found to be significant on the concentrations of Fe and Pb; their concentrations were found to increase in all the organs. However, the concentrations of Cu and Zn were found to be decreased significantly in the liver. In the animals given Fe, Cu, or Zn supplementation along with motor exhaust, the percentage change in the concentration of Pb in lungs was decreased, and that of Fe was increased significantly. In kidney, no significant change was observed for the animals given Cu and Zn, whereas for animals given Fe, the level of Pb decreased significantly. In liver, the reduction in the level of Zn in the exhaust-exposed animals was made up and the level of Pb was reduced following Zn supplementation. These results clearly indicate that Fe and Zn play an important role in Pb metabolism and tend to lower the absorption of Pb. The effect of Fe is more pronounced than that of Zn, whereas the effect of Cu seems to be insignificant.

Determination of bromine and iodine in normal tissues from Beijing healthy adults.

The contents of bromine and iodine in samples of heart, liver, spleen, lung, muscle, and hair from healthy adults living in Beijing, China, were determined using epithermal neutron activation analysis. The results indicate that the contents of bromine in lung and iodine in liver are higher than those in other tissues, except human hair. The bromine contents in Beijing human tissues are significantly lower than those in other countries. The contents of iodine are slightly lower than those in other countries, but the difference is not significant. Three biological standard reference materials were simultaneously determined with the samples, and our results agree well with the certified values.

Effects of inhaled methyl bromide gas on the metabolic system and kinetics of bromine ion in rats.

Wistar male rats were exposed to 2000 ppm of methyl bromide gas for one hour (single exposure experiment) or 300 ppm of the gas for 6 hours a day, 3 days a week for 4 or 8 weeks (repeated exposure experiment) to investigate the metabolism of inhaled methyl bromide. After the exposure was completed, the bromine ion concentration in serum was measured up to 60 days. The serum bromine ion concentration was determined by a headspace gas chromatography-mass spectrometry after converting bromine ion to methyl bromide by adding dimethyl sulfate in the serum samples. In the single exposure experiment, the bromine ion concentration decreased quickly within one day after the end of the exposure, and then began to decrease gradually. In the repeated exposure experiment, on the other hand, the bromine ion concentration decreased almost exponentially. A two-compartment model was applied to analyze the clearance rate of bromine ion. The biological half time of serum bromine ion was 9.1 days for the single exposure and 5.4 days for the repeated exposure. The amount of cytochrome P450 (CYP) in liver microsomes was measured after the end of exposure. CYP in liver was not significantly different after the repeated exposure but it decreased after the single exposure.

A comparison of chloride, bromide, and sucrose dilution volumes in neonatal pigs.

Use of 36Cl, 82Br, and [3H]sucrose to estimate extracellular water volume was evaluated in 14 piglets (7-14 days old). 36Cl and 82Br were distributed in approximately the same volume, but a period of 5-6 hr after injection was required to reach equilibrium in the neonatal pig. Dilution volumes calculated before equilibration (2-5 hr) for 36Cl (326 +/- 11 ml/kg) and 82Br (328 +/- 13 ml/kg) were different from equilibration (6-8 hr) phase volumes (356 +/- 13 ml/kg and 355 +/- 13 ml/kg, respectively; P less than 0.001). A 3-hr sample estimated the same volume distribution calculated by extrapolation of the 6- to 8-hr period because of the relationship between the two slopes of the plasma clearance curves. After the 82Br and 36Cl had achieved equilibration, each was distributed in a volume equivalent to total body chloride space (362 +/- 29 ml/kg) measured by neutron activation; no statistical differences were found (P = 0.6). The early equilibration phase measured a 10% smaller, faster exchangeable fraction of total body Cl. Sucrose dilution volume (332 +/- 19 ml/kg) required multiple plasma samples for extrapolation and measured a dilution volume 7% smaller (P less than 0.05) than total body chloride space.

Chloride channels activated by hypotonicity in N2A neuroblastoma cell line.

By using the patch-clamp technique we have shown that, in hypotonic extracellular solutions, the mouse neuroblastoma cells Neuro2A (N2A) develop ionic currents mediated by a chloride-selective channel which is also permeable to other anions in accordance with the permeability sequence: I->Br->Cl->gluconate->glutamate-. The currents persist for several hours when Mg-ATP is present in the recording pipette but occur only transiently in the absence of Mg-ATP. Typical blockers of anions channels such as La3+ and Zn2+ do not affect the hypotonicity-activated channel; conversely, the stilbene sulfonate-derivatives, 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid (SITS) and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), reversibly inhibit the channel in a voltage-dependent manner. Also intact cells exposed to hyposmotic solutions activate volume-regulation mechanisms which decrease the transient volume increase that develops immediately after the application of the hyposmotic challenge. Since N2A neurons have been used as an expression system of exogenous channels, the presence of osmolarity-regulated channels in these cells is an important aspect that deserves the attention of researchers who may wish to express and study the properties of transport proteins in this cell line.

Actin filament organization is required for proper cAMP-dependent activation of CFTR.

Previous studies have indicated a role of the actin cytoskeleton in the regulation of the cystic fibrosis transmembrane conductance regulator (CFTR) ion channel. However, the exact molecular nature of this regulation is still largely unknown. In this report human epithelial CFTR was expressed in human melanoma cells genetically devoid of the filamin homologue actin-cross-linking protein ABP-280 [ABP(-)]. cAMP stimulation of ABP(-) cells or cells genetically rescued with ABP-280 cDNA [ABP(+)] was without effect on whole cell Cl(-) currents. In ABP(-) cells expressing CFTR, cAMP was also without effect on Cl(-) conductance. In contrast, cAMP induced a 10-fold increase in the diphenylamine-2-carboxylate (DPC)-sensitive whole cell Cl(-) currents of ABP(+)/CFTR(+) cells. Further, in cells expressing both CFTR and a truncated form of ABP-280 unable to cross-link actin filaments, cAMP was also without effect on CFTR activation. Dialysis of ABP-280 or filamin through the patch pipette, however, resulted in a DPC-inhibitable increase in the whole cell currents of ABP(-)/CFTR(+) cells. At the single-channel level, protein kinase A plus ATP activated single Cl(-) channels only in excised patches from ABP(+)/CFTR(+) cells. Furthermore, filamin alone also induced Cl(-) channel activity in excised patches of ABP(-)/CFTR(+) cells. The present data indicate that an organized actin cytoskeleton is required for cAMP-dependent activation of CFTR.