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PubMed2003

The effect of manganese chloride on gentamicin-induced nephrotoxicity in rats.

The aim of this study was to investigate the effects of manganese chloride on gentamicin-induced nephrotoxicity in rats. Thirty-six adult Wistar Albino rats were divided into six equal groups. They were injected with gentamicin sulfate (100 mg kg(-1) per day i.p.) and manganese chloride (2 or 20 mg kg(-1) per day i.p.) and gentamicin together with manganese chloride for 6 days. The animals were killed 24 h after the last injection. Nephrotoxicity was biochemically and histopathologically evaluated. The concentrations of creatinine, urea, sodium and potassium in plasma, malondialdehyde (MDA) and reduced glutathione (GSH) levels, glutathione peroxidase (GSH-Px) and catalase (CAT) activities in kidney tissue were determined. Administration of gentamicin to rats induced a marked renal failure, characterized with a significant increase in plasma creatinine and urea concentrations. A significant increase in kidney MDA and a decrease in GSH concentrations were observed in gentamicin-treated rats. No change was observed in the activities of GSH-Px and CAT in rats treated with gentamicin alone. Administration of the low dose of manganese (Mn2+) produced amelioration in biochemical indices of nephrotoxicity in plasma and kidney tissue when compared to gentamicin group. The histological signs of renal proximal tubules followed a similar pattern. The high dose of Mn2+ (20 mg kg(-1)) caused an opposite effect on nephrotoxicity induced by gentamicin, causing exacerbation in the tubular necrosis. The results suggest that low dose of Mn2+ may have an antioxidant effect in kidneys of gentamicin administrated rats, but its high doses had no beneficial effect.

Animals↗
PubMed1985

The effect of substrate and potassium on the inhibitory kinetics of MnCl2 on the enzyme K+-p-nitrophenyl phosphatase in rat brain.

The effect of Mn2+, a divalent metal, on the enzyme K+-p-nitrophenyl phosphatase (K+-PNPPase) was studied in rat brain. The metal was found to be a moderate inhibitor of the enzyme, with an I50 of approximately 480 microM. The inhibition was pH dependent, but not temperature dependent. On measurement of the inhibition with varying concentrations of PNPP (1-5 mM), the I50 value remained constant. However, when the inhibition was measured with K+ (5-20 mM), the I50 value increased from 130 microM to 490 microM, suggesting that K+ antagonized the effect of Mn2+. In kinetic studies, Mn2+ inhibited the enzyme in a non-competitive manner with respect to PNPP. The Km remained constant (2.9), but the Vmax was decreased from 5.0 to 1.6. However, with respect to K+, the inhibition was competitive, as the concentration for half maximal activation (K0.5) increased from 1.3 to 8.9 mmol l-1 with 1 mM of MnCl2, suggesting that the apparent affinity of K+ for the enzyme was decreased. The apparent Vmax was not affected. The degree of cooperactivity (n) measured as the slope of the Hill plot remained unaltered (1.9 +/- 0.2) over the entire concentration range of MnCl2 tested.

4-Nitrophenylphosphatase↗
PubMed1998

Nitric oxide donors inhibit iodide transport and organification and induce morphological changes in cultured bovine thyroid cells.

Nitric oxide (NO) has been proposed as an intracellular signal in the thyroid. The NO effect on function and morphology of bovine thyroid follicles in culture was analyzed by using the NO donors sodium nitroprusside (SNP) and S-nitrosoglutathione (GSNO). Both NO donors induced a concentration-dependent NO release measured by the nitrite accumulation in the culture medium. The SNP (10 to 500 micromol/L) treatment for 24 hours significantly inhibited the uptake, organification and transport of iodide in a concentration-dependent manner. When SNP (50 micromol/L) was withdrawn from the culture medium after 24 hours' incubation, iodide uptake and organification were partially recovered at 24 hours and reached the control value at 48 hours, indicating a reversible effect of SNP. A possible involvement of cyanide in the SNP inhibitory effect was excluded because incubation of follicles with potassium cyanide (KCN) at concentrations estimated to be present in the medium (40 and 80 micromol/L) for 24 hours did not modify iodide uptake and organification. The GSNO (10 to 500 micromol/L) treatment for 24 hours also reduced the iodide uptake, organification and transport in a concentration-dependent manner. A significant inhibition of iodide organification was induced after incubation with 1000 micromol/L of N2, 2'-O-dibutyrylguanosine 3':5'-cyclic monophosphate ([Bu]2cGMP). Morphological evaluation by light microscopy revealed that the incubation with NPS or GSNO (500 micromol/L) produced cellular dispersion with loss of follicular cell aggregates that was evident at 96 hours exposure. Cell viability was not altered by 10-500 micromol/L SNP or GSNO (80% to 85%). We concluded that long-term NO exposure induces functional and morphological modifications compatible with a loss of differentiation in thyroid follicles. These observations further support a role of NO in the regulation of the thyroid function.

Animals↗
PubMed1988

Effects of leukotriene D4 on the mechanical and electrical properties of guinea-pig isolated trachealis.

1. The effects of leukotriene D4 (LTD4) on mechanical and electrical activity were examined in guinea-pig isolated trachealis muscle and compared with two other bronchoconstrictors, methacholine and potassium chloride (KCl). 2. LTD4 elicited concentration-dependent increases in tension in trachealis muscle which were slower in time course than responses induced by either methacholine or KCl. The maximum response to LTD4 was approximately 85% of the methacholine maximum. 3. At a concentration close to the EC50 for tension changes, LTD4 had no significant effect on either transmembrane potential or slow wave activity recorded in single trachealis cells. 4. At a concentration close to the EC90 for tension changes, LTD4 caused significant membrane depolarization, transiently reduced the amplitude and increased the frequency of slow wave discharge and ultimately abolished slow wave discharge. LTD4-induced depolarization was less marked, and developed more slowly, than that evoked by either methacholine or KCl. 5. These results show that LTD4 can elicit substantial increases in tension without altering transmembrane potential and are consistent with the view that LTD4 initiates contraction mainly through potential-independent mechanisms. However, at high concentrations the depolarization evoked by LTD4 allows the possibility that potential-dependent mechanisms may contribute to the spasm.

Airway Resistance↗
PubMed1992

Slow voltage-dependent block of sodium channels in crayfish nerve by dihydropyrazole insecticides.

Previous current-clamp work has shown that dihydropyrazole insecticides block sodium channels in tonic sensory receptors and in axons depolarized by high K+ external solutions and that hyperpolarization removes the block [Pestic. Sci. 28:389-411 (1990)]. Voltage-clamp studies on internally perfused crayfish giant axons were done to confirm and extend these observations. At -100 mV dihydropyrazoles had little effect on the sodium current, but at more depolarized potentials they blocked it from either face of the membrane. The onset of block following a holding potential change or during wash-in of a dihydropyrazole was very slow, with a time constant of several minutes, and, although block could be removed with a similar time course by hyperpolarization, the effects of the insecticides could not be reversed by prolonged washing. Dihydropyrazoles did not affect delayed rectifier potassium currents in the axon. The voltage-dependent block could be described as a uniform shift of the steady state (slow) sodium inactivation (S infinity) curve in the direction of hyperpolarization, indicative of selective binding to inactivated states of the channel. Using hyperpolarizing prepulses to remove slow inactivation, block of sodium channels by dihydropyrazoles could be measured directly at holding potentials as positive as -50 mV, and it could be demonstrated that block saturated near -70 mV, consistent with a dependence on slow inactivation. The data were fit to a model tha assumes the dihydropyrazole binds to the slow-inactivated state of the channel on a one to one basis. Dissociation constants obtained from this analysis were similar to those obtained from analysis of inhibition of the binding of [benzoyl-2,5-3H]-batrachotoxinin A 20-alpha-benzoate by the same dihydropyrazoles. In axons whose fast or slow inactivation gates had been removed by N-bromoacetamide or trypsin, respectively, dihydropyrazoles still blocked sodium current, indicating that dihydropyrazoles can block the channel as well as enhance the normal slow inactivation process.

Animals↗
PubMed1984

Potassium-p-nitrophenyl phosphate interactions with (Na+ + K+)-ATPase. Their relevance to phosphatase activity.

The K+-dependent p-nitrophenylphosphatase activity catalyzed by purified (Na+ + K+)-ATPase from pig kidney shows substrate inhibition (Ki about 9.5 mM at 2.1 mM Mg2+). Potassium antagonizes and sodium favours this inhibition. In addition , K+ reduces the apparent affinity for substrate activation, whereas p-nitrophenyl phosphate reduces the apparent affinity for K+ activation. In the absence of Mg2+, p-nitrophenyl phosphate, as well as ATP, accelerates the release of Rb+ from the Rb+ occluded unphosphorylated enzyme. With no Mg2+ and with 0.5 mM KCl, trypsin inactivation of (Na+ + K+)-ATPase as a function of time follows a single exponential but is transformed into a double exponential when 1 mM ATP or 5 mM p-nitrophenyl phosphate are also present. In the presence of 3 mM MgCl2, 5 mM p-nitrophenyl phosphate and without KCl the trypsin inactivation pattern is that described for the E1 enzyme form; the addition of 10 mM KCl changes the pattern which, after about 6 min delay, follows a single exponential. These results suggest that (i) the shifting of the enzyme toward the E1 state is the basis for substrate inhibition of the p-nitrophenylphosphatase activity of(Na+ + K+)-ATPase, and (ii) the substrate site during phosphatase activity is distinct from the low-affinity ATP site.

Animals↗
PubMed2000

Effects of infusion of glucose-insulin-potassium on myocardial function after a recent myocardial infarction.

UNLABELLED: We studied the effects of glucose, insulin, and KCl infusion (GIK), on regional myocardial perfusion and function by 99m-Tc-tetrofosmin-gated SPECT. METHODS: We studied 21 male patients with their first uncomplicated acute myocardial infarction (AMI). All patients underwent a rest and submaximal stress before and after 24-hour infusion of GIK-solution (group A) or saline solution (group B). RESULTS: Group A showed better stress tolerance and ischaemic threshold improvement after GIK infusion whilst no statistical differences were found between basal and post-infusion test in group B. At first the stress test in group A, of the 192 segments analysed, 52 (27%) showed reversible perfusion defect. In group B, of 144 segments analysed, 31 (21%) showed reversible perfusion defect. A post-infusion analysis in group A showed a post-GIK end-diastolic significant count improvement in 21 segments, and a post-GIK end-systolic count improvement in 22 segments. In group B, perfusion increase was observed only in 4 segments, whilst systolic thickening increase was observed only in 1 segment. CONCLUSION: These data demonstrate the efficacy of GIK infusion to improve regional myocardial perfusion and function mainly in segments adjacent to the recently infarcted area.

Adult↗
PubMed1998

Substrate-dependent cadmium toxicity affecting energy-linked K+/86Rb transport in Staphylococcus aureus.

Bacteria accumulate high amounts of potassium in the cytoplasm. For studying transport of K+ (with 86Rb as a marker) in bacteria (Staphylococcus aureus 17810S), the cells were depleted of the internal K+ pool by a DNP treatment. Kinetics and energetics of 86Rb transport was assayed with glucose as an exogenous energy source. It was shown that 86Rb uptake proceeded via a low affinity K+ transport system with an apparent K(m) of 2.3 mmol/L Rb+. Studies with the lipophilic cation TPP+ (tetraphenylphosphonium), the protonophore CCCP (carbonyl cyanide 3-chlorophenylhydrazone) and inhibitors (HQNO--2-heptyl-4-hydroxyquinoline N-oxide; iodoacetate) indicated that 86Rb transport was driven by delta psi (membrane potential) generated via the respiratory chain. The effect of Cd2+ on 86Rb transport was assayed with two energy donors--glucose and L-lactate. It was found that Cd2+ strongly inhibited delta psi-dependent 86Rb transport energized by cadmium-sensitive glucose oxidation, but was not toxic when cadmium-insensitive L-lactate was used as an energy source. The mechanism of these differential, substrate-dependent effects of Cd2+ on 86Rb transport is discussed.

2,4-Dinitrophenol↗
PubMed1982

Dimethylphosphorothioates. Reaction with malathion and effect on malathion toxicity.

Five dimethylphosphorothioates were tested for their toxicity to rats, potentiation of malathion toxicity in rats, inhibition of carboxylesterase in vitro, and reaction with malathion in vitro. The compounds were: potassium salts of (CH3S)2P(O)O-(I), (CH3O)(CH3S)P(O)S-(II), (CH3O)2P(O)S-(III), (CH3O)2P(S)S-(IV), and (CH3O)(CH3S)P(O)O-(V). The dimethylphosphorothioates are not toxic to rats (up to 1 g/kg, orally), they do not potentiate malathion toxicity in rats, and do not inhibit carboxylesterase activity in vitro (up to 1 mM concentrations). However, when the S-acid diesters (II, III, IV) are incubated with malathion for serveral days at room temperature or for several hours at 50 degrees C they become methylated forming the trimethylphosphorothioates OSS-trimethyl phosphorodithioate, OOS-trimethyl phosphorothioate and OOS-trimethyl phosphorodithioate respectively, which potentiate malathion toxicity. Furthermore, these same acid diesters increase the rate of isomerization of malathion into OS-dimethyl-S-(1,2-dicarbethoxyethyl) phosphorodithioate (isomalathion) particularly, diester IV. The formation of the trimethylphosphorothioates and isomalathion from the interaction of the S-acid diesters with malathion was determined by thin layer chromatography (TLC), gas chromatography and mass spectrometry and could be detected by in vitro inhibition of carboxylesterase. TLC methods can detect 1 mg of the trimethylphosphorothioates and isomalathion per gram malathion.

Animals↗
PubMed2005

Evidence for a selective prefrontal cortical GABA(B) receptor-mediated inhibition of glutamate release in the ventral tegmental area: a dual probe microdialysis study in the awake rat.

Glutamate-containing pyramidal neurons in the medial prefrontal cortex (mPfc) project to the ventral tegmental area (VTA) where they synapse on mesocorticolimbic dopamine containing cell bodies and GABA interneurons. In the present study we employed dual probe microdialysis in intact conscious rat brain to investigate the effects of intra-mPfc perfusion with a depolarising concentration of potassium chloride (KCl) (100 mM, 20 min) alone and in the presence of local GABA(A) and GABA(B) receptor blockade on VTA glutamate release. Intra-mPfc KCl transiently increased VTA glutamate release (+71.48+/-14.29%, 20 min). Intra-mPfc perfusion with a concentration of the GABA(A) receptor antagonist bicuculline (10 microM, 120 min) did not influence the intra-mPfc KCl-induced increase in VTA glutamate release (+102.35+/-33.61%, 20 min). In contrast, intra-mPfc perfusion with a concentration of the GABA(B) receptor antagonist CGP35348 (100 microM, 120 min) which when given alone did not influence basal glutamate levels in the VTA was associated with an enhanced KCl-induced stimulation of VTA glutamate release (+375.19+/-89.69%, 40 min). Furthermore, this enhancement was reversed in the presence of the selective GABA(B) receptor agonist baclofen (10 microM, 120 min). The present findings suggest a key role for the prefrontal cortex in the regulation of glutamate release in the VTA. Furthermore, we demonstrate a selective cortical GABA(B) receptor-mediated inhibition of glutamate transmission in the VTA. These findings may be important in the context of abnormalities in amino acid neurotransmission at the network level in schizophrenia.

Animals↗
PubMed2005

Effects of ATP-sensitive potassium channel activators diazoxide and BMS-191095 on membrane potential and reactive oxygen species production in isolated piglet mitochondria.

Mitochondrial ATP-sensitive potassium (mitoK(ATP)) channel openers protect the piglet brain against ischemic stress. Effects of mitoK(ATP) channel agonists on isolated mitochondria, however, have not been directly examined. We investigated the effects of K(ATP) channel openers and blockers on membrane potential and on the production of reactive oxygen species (ROS) in isolated piglet mitochondria. Diazoxide and BMS-191095, putative selective openers of mitoK(ATP), decreased the mitochondrial membrane potential (delta psi(m)). On a molar basis, diazoxide was less effective than BMS-191095. In contrast, diazoxide but not BMS-191095 increased ROS production by mitochondria. Since diazoxide also inhibits succinate dehydrogenase (SDH), we examined the effects of 3-nitropropionic acid (3-NPA), an inhibitor of SDH. 3-NPA failed to change the delta psi(m) but increased ROS production. Inhibitors of K(ATP) channels did not affect resting delta psi(m) or ROS production, but glibenclamide and 5-hydroxydecanoate (5-HD) blocked effects of diazoxide and BMS-191095 on delta psi(m) and diazoxide effects on ROS production. We conclude that BMS-191095 has selective effects on mitoK(ATP) channels while diazoxide also increases ROS production probably via inhibition of SDH.

Adenosine Triphosphate↗
PubMed1998

Bone marrow and liver mutagenesis in lacZ transgenic mice treated with hexavalent chromium.

The mutagenic effects of the hexavalent chromium compound K2CrO4 in lacZ transgenic mice (Muta Mouse) were investigated at two sampling times. K2CrO4 was administered intraperitoneally to five male mice per treatment group at a single dose of 40 mg/kg. The animals were sacrificed on days 1 and 7 after the treatment. Mutant frequencies in the bone marrow and liver were analyzed by the positive selection method using Escherichia coli C (galE-) strain and phenyl beta-D-galactoside. K2CrO4 induced a significant increase in mutant frequency in the bone marrow on day 1, but not on day 7 after the treatment. In the liver, on the other hand, a significant induction in the mutant frequency was seen on day 7, whereas no induction was observed on day 1. The reason for the different responses to the mutagenic activity of K2CrO4 between these organs may be related to their cell turnover rates. The mutations induced by K2CrO4 in the bone marrow may have occurred in more differentiated cells than stem cells, and the rapid proliferative activity may have caused a rapid decrease in mutated cells by day 7. These results suggest that experiments on mutagenesis should be done with more than one sampling point, a short expression time in addition to a longer one, so as to detect mutations induced in organ with high cell proliferation.

Animals↗
PubMed1994

Differences in the Cs block of baclofen and 4-aminopyridine induced potassium currents of guinea pig CA3 neurons in vitro.

Single-electrode current- and voltage-clamp techniques were employed to study responses elicited by (-)baclofen or gamma-aminobutyric acid (GABA) and 4-aminopyridine (4-AP) induced inhibitory postsynaptic potentials in CA3 pyramidal neurons in guinea pig hippocampal slices. All drugs were applied by the bath to submerged slices in which fast synaptic transmission was blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (10 microM), bicuculline (50 microM), and picrotoxin (50 microM). (-)Baclofen (0.5 microM) and GABA (1 mM) induced equivalent-sized hyperpolarizations and input resistance decreases. The agonist induced hyperpolarization or current and 4-AP induced hyperpolarizations or currents (4-AP induced K-IPSPs or IPSCs) reversed in sign near the K-equilibrium potential (EK). The GABAB receptor antagonists, OH-saclofen (500 microM) and CGP 35348 (100 microM), reduced (-)baclofen responses, and 4-AP induced K-IPSPs, suggesting that they were mediated by GABAB receptors. Intracellular tetraethylammonium-, and extracellular barium-ions (1 mM) diminished the (-)baclofen induced current and 4-AP induced K-IPSCs. Intracellular Cs-ions blocked the (-)baclofen induced outward current at resting membrane potential but did not grossly affect the inward current recorded at membrane potentials negative to EK. 4-AP induced inwardly or outwardly directed K-IPSCs were not blocked by intracellular Cs-ions. Extracellular Cs-ions (5 mM) blocked the (-)baclofen induced inward K-current, but did not block 4-AP induced inwardly directed K-IPSCs. In conclusion, we found differences in the Cs block of activated by (-)baclofen or the endogenous transmitter GABA.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗
PubMed1981

Transient and steady-state kinetic studies of sodium-potassium adenosine triphosphatase using beta-(2-furyl)acryloyl phosphate as chromophoric substrate assay.

A convenient and highly specific continuous spectrophotometric assay for sodium-potassium adenosine triphosphate activity utilizing the rapidly hydrolyzed and high-affinity chromophoric substrate beta-(2-furyl)acryloyl phosphate (FAP) is described. The Na/K-ATPase-catalyzed hydrolysis of FAP is faster than that for ATP under all ionic conditions. The rate is neither inhibited nor activated by Na+; it is dependent on [K+] and on [Mg2+]. The hydrolysis of FAP to furylacrylate is accompanied by a large shift in the UV absorbance maximum. The spectrum of FAP, but not furylacrylate, is sensitive to noncovalent ligation with Mg2+, a happenstance which permits the identification of Mg2+FAP, and consequently allows for a probe of the role of Mg2+ in the catalysis. Mg2+ binding to the active site is essential for catalysis. MgFAP is more tightly bound to the site than is FAP2-, but the complex is not obligatory for catalysis. The formation of a phosphoryl-enzyme intermediate is not evident in the reaction of FAP with the enzyme. Transient kinetic experiments, utilizing an excess of MgFAP, demonstrate a unique steady-state rate-limiting production of furylacrylate. These results indicate that the pathway demonstrated with ATP is not appropriate to the FAPase mechanism. The results suggest that acyl phosphates are good "phosphatase" substrates either because they are analogues of the phosphatase-specific phosphoryl-enzyme or because they react exclusively with the isomerized "E2" form of the enzyme.

Acrylates↗
PubMed1982

Interactions between three slow potassium responses controlled by three distinct receptors in Aplysia neurones.

1. A voltage clamp study was made of the K(+) permeability increases produced in certain identifiable neurones of the cerebral ganglion of Aplysia by any one of three distinct agonists (carbachol, histamine and dopamine).2. The three K(+) responses involve three distinct receptors, as shown by the selective effects of reversible antagonists (Gruol & Weinreich, 1979a) as well as by the differential, irreversible effects of trimethyloxonium (TMO) ions.3. Prolonged exposure of the neurones to one of the agonists reduces the response to the same agonist (desensitization) and, over the low concentration range, doubling the concentration of an agonist leads to supra-linear summation (potentiation).4. Prolonged exposure of the neurones to one of the agonists also reduces the response to the other agonists (cross-desensitization) and combined application of two agonists reveals cross-potentiation.5. The time course of desensitization (onset and decay) was the same for the histamine and carbachol responses and, except at very high concentration, was indistinguishable from that of cross-desensitization. Likewise, potentiation was similar in the two agonist systems and did not differ significantly from cross-potentiation.6. The results can be interpreted by assuming that the responses to the three agonists involve specific steps followed by common reaction steps, and that some of the common reaction steps control both potentiation and desensitization.7. The responses to carbachol and histamine differ in their voltage sensitivity. This suggests that one or more of the specific steps are voltage-sensitive.8. Although an increase of the intracellular Ca(2+) concentration can itself open K(+) channels, and also inhibit the responses to the three agonists, an increase of internal Ca(2+) does not appear to play an important role either in the development of the response or in the desensitization process.

Acetylcholine↗
PubMed1986

Hypersensitive teeth. Part II: Treatment.

If the hydrodynamic theory for pain transmission were accepted, occlusion of the patent dentinal tubules would appear to be essential for treatment efficacy. There are many compounds with seemingly varied chemical forms that have been shown to be effective. Their exact mode of action however, is not clearly defined because well-designed, nonbiased, and controlled comparison studies between agents are lacking. The various toothpastes may have ingredients that actually occlude patent tubules or they may cause secondary desensitization by irrational or abrasive action. In any pain study, the nature of the placebo effect and other psychogenic factors play a significant role. Fluoride preparation with and without iontophoresis has been shown to alter tubule structure and form microprecipitates. The natural desensitization process, although slow, is nature's protection, allowing dentinal sclerosis of secondary dentin formation. Although the resin-adhesive systems, especially the new light-cured dentin bonding agents, appear immediately to be effective, the effect on the pulp remains unknown. Perhaps a combination of iontophoresis with sodium fluoride and light-cured dentin bonding material may yield protection and desensitization at a high level of predictability. With the population trends toward a more geriatric society, further research, knowledge, and understanding of dentinal hypersensitivity is of paramount importance. The expected increase in longevity of the dentition suggests that dentin exposure and sensitivity will increase as a clinical problem. There is a clear time-age relationship involved in gingival recession, erosion and attrition of the teeth, and the need for periodontal surgical therapy. For total comprehensive care, patient comfort is important and should be provided along with sound periodontal health and ideal restorative function.

Adhesives↗
PubMed2003

Occupational asthma due to persulfate salts: diagnosis and follow-up.

BACKGROUND: Persulfate salts have been identified as a cause of occupational asthma (OA). The aim of the present study was to describe the clinical characteristics, diagnostic testing results, and follow-up of eight patients with OA that was triggered by these chemical compounds. METHODS: Eight patients with OA due to exposure to persulfate salts were studied. Immunologic, lung function, and specific bronchial challenge tests (SBCTs) were performed in all patients. Once their condition had been diagnosed, the patients were seen every 1, 3, and 6 months for a mean duration of 18 months. RESULTS: The mean time of exposure to persulfate salts up to diagnosis was 15 years (range, 3 to 27 years), and mean time that had elapsed between symptom onset and diagnosis was 38 months (range, 3 to 120 months). Three patients were smokers, six patients presented with rhinitis prior to asthma in relation to persulfate exposure, and three presented with dermatitis. The results of total IgE tests were positive in six patients, and the results of skin-prick tests for detection of persulfate salts were positive in five of these patients. The results of a SBCT was positive in the seven patients in whom it was performed. Symptoms persisted in all but one patient and required medical treatment. CONCLUSIONS: The results suggest that the reliable diagnosis of OA due to persulfate salts must be based on the specific challenge test until further experience has been acquired. Despite avoiding exposure, patients continued with symptoms and required treatment for the control of symptoms. Finally, a dependent IgE mechanism appears to be implicated in the pathogenesis of OA due to exposure to persulfate salts.

Adult↗
PubMed1991

[Nitrate and nitrite levels in daily food rations of children from the rural Puławy regions].

In the region of Puławy where the operation of the Nitrogen-Compound Manufacturing Plant has lead to an increase in nitrogen compound emission to the environment, nitrate and nitrite contents in daily food rations of children were determined. Daily food rations of children aged 8-9 and 12-13 years were collected from individual farms in four villages situated in the vicinity of the Nitrogen Plant, as well as--for control--from individual farms in Janowiec, a village distant from this Plant. Nitrate and nitrite contents were assayed in 300 daily food rations taken in spring and autumn. Nitrate was reduced to nitrite on a cadmium column whereupon it was determined colorimetrically using sulphanilic acid and N-1-napthyl-ethylenediamine. It was found that in the group of younger children as many as 70%, on the average, of the examined food rations displayed nitrate contents exceeding the admissible levels. In the group of the 12-13 years old children, the percentage of daily food rations whose nitrate content exceeded the admissible level was lower, averaging ca. 30% of all rations examined. The percentage of the daily food rations in which the nitrite content was higher than admissible level was closely similar in both groups of children, averaging ca. 30% of all rations examined. Food rations collected in spring, as compared with those taken in autumn, contained significantly greater amount of nitrate. In both periods of studies, nitrate contents were greater in the food rations from the farms situated near the Nitrogen Plant than in the food rations from farms in Janowiec.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗