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PubMed1987

A model of pulmonary granulomata induced by beryllium sulfate in the rat.

In humans beryllium is known to cause pulmonary granulomata which are histologically indistinguishable from sarcoidosis. There is some evidence in man that beryllium-induced pulmonary granulomata are immunologically mediated. We set out to develop an animal model to study the immunopathogenesis of beryllium-induced granulomatous lung disease. Beryllium sulfate (BeSO4) was injected intratracheally (i.t.) into F344 rats previously immunized to BeSO4. This results in well-formed, sarcoid-like lung granulomata at 6 weeks post BeSO4. There was a conspicuous presence at 4 weeks post BeSO4 of numerous, perivascularly located Langhans' giant cells which preceded the development of well-formed granulomas at 6 weeks. Rats were sacrificed at 4, 6, 8 and 12 weeks after i.t. BeSO4. At the time of sacrifice bronchoalveolar lavage (BAL) was performed; B and T (W3/25+ helper 0X8+ suppressor/cytotoxic) lymphocyte populations were quantitated and compared to lymphocyte populations obtained from lung tissue. Both B and T cells were significantly elevated in lung tissue post BeSO4. At 4 weeks when granulomata were just developing, a W3/25+ to 0X8+ ratio of 20:1 in lavage and 2:1 in lung tissue was seen. At 6 weeks when granulomata were well-formed there was a predominance of W3/25+ cells in lavage but not in lung tissue. At 8 and 12 weeks, when the granulomata were regressing, lavage fluid still contained a W3/25+ predominance in contrast to lung tissue which contained a predominance of 0X8+ cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Formation of the stable myosin-ADP-aluminum fluoride and myosin-ADP-beryllium fluoride complexes and their analysis using 19F NMR.

The effects of aluminum fluoride and beryllium fluoride on smooth muscle myosin and its subfragments were studied. Mg(2+)-ATPase activity was inhibited in the presence of aluminum fluoride (beryllium fluoride). [3H]ADP bound to heavy meromyosin (HMM) in the presence of aluminum fluoride (beryllium fluoride) and was not dissociated after 3 days of dialysis demonstrating that [3H]ADP was trapped in HMM. These results suggest the formation of a stable HMM-ADP-fluoroaluminate (fluoroberyllate) complex. The intrinsic tryptophane fluorescence intensity was increased in the presence of ADP and aluminum fluoride (beryllium fluoride). Acto-S1 was dissociated upon the formation of S1-ADP-fluoroberyllate and actin destabilized S1-ADP-fluoroberyllate complex, while S1-ADP-fluoroaluminate failed to bind to actin. Furthermore, when S1 formed the complex with actin, nucleotide trapping did not occur in the presence of fluoraluminate. These results indicated that the myosin-ADP-fluoroberyllate complex resembles a weak binding state while myosin-ADP-fluoroaluminate complex is a distinct conformation although the binding to actin was also weak. The structure of the ternary complex was investigated using 19F NMR. The 19F NMR spectrum of the S1-ADP-fluoroaluminate complex showed a peak at -66.7 ppm which is due to the binding of fluoraluminate to S1. The peak was not observed when 5'-adenylylimidodiphosphate was substituted for ADP suggesting that aluminum fluoride plays a role as a phosphate analogue. The stoichiometry of the bound fluoride was determined to be 3.8 mol/mol S1 suggesting that the bound species is AlF-4.

Adenosine Diphosphate↗
PubMed1997

Synthesis, (9)Be NMR Spectroscopy, and Structural Characterization of Sterically Encumbered Beryllium Compounds.

The use of the terphenyl substituent -C(6)H(3)-2,6-Mes(2) (abbreviated Ar) has permitted the synthesis of several new low-coordinate beryllium compounds. Reaction of 1 equiv of LiAr with BeCl(2)(OEt(2))(2) or BeBr(2)(OEt(2))(2) (1) gives the monomeric complexes ArBeX(OEt(2)) (X = Cl (2); Br (3) featuring three-coordinate berylliums. Treatment of 2 with 1 equiv of LiSMes (Mes = -C(6)H(2)-2,4,6-t-Bu(3)) affords the three-coordinate thiolate derivative ArBeSMes(OEt(2)) (4). The reaction of 2 with LiNHPh, LiNHSiPh(3), or LiN(SiMe(3))(2) affords the unstable dimer (ArBeNHPh)(2) (5) or the monomers ArBeNHSiPh(3)(OEt(2)) (6) and ArBeN(SiMe(3))(2) (7). The last is the first example of a two-coordinate beryllium center in the solid state. The addition of 1 equiv of 2 to NaMo(eta(5)-C(5)H(5))(CO)(3) gives the isocarbonyl complex Ar(THF)(2)Be(OC)(3)Mo(eta(5)-C(5)H(5)) (8), which features four-coordinate beryllium bound to Ar, two THF ligands, and an oxygen from one of the molybdenum-bound carbonyls. Reaction of 2 with a 1:1 mixture of LiN(SiMe(3))(2) and PhCN affords the six-membered-ring compound PhC(NSiMe(3))(2)(BeCl)(2)N(SiMe(3))(2) (9) and the four-coordinate monomer Be{(NSiMe(3))(2)CPh}(2) (10). Compounds 1-10 were characterized by X-ray crystallography, and 1 and 4 and 6-10 were also characterized by (1)H, (9)Be, and (13)C NMR spectroscopy. X-ray data at 130 K (1-9) or 185 K (10) with Mo Kalpha (lambda = 0.710 73 Å) (1, 2a, 3, 7, 8) or Cu Kalpha (lambda = 1.541 78 Å) (2b, 4-6, 9, 10). BeBr(2)(OEt(2))(2) (1), a = 11.690(5) Å, b = 10.191(3) Å, c = 12.131(5) Å, beta = 114.67(3) degrees, V = 1313.3(9) Å(3), space group P2(1)/n, Z = 4, R(1) = 0.062; ArBeCl(OEt(2)) (2a), a = 13.136(3) Å, b = 13.877(3) Å, c = 28.092(6) Å, V = 5121(2) Å(3), space group Pbca, Z = 8, R(1) = 0.058; ArBeCl(OEt(2)) (2b), a = 8.857(1) Å, b = 8.8977(9) Å, c = 18.198(7) Å, alpha = 86.437(8) degrees, beta = 82.677(8) degrees, gamma = 62.405(7) degrees, V = 1260.5(2) Å(3), space group P&onemacr;, Z = 2, R(1) = 0.048; ArBeBr(OEt(2)) (3), a = 8.873(5) Å, b = 8.847(5) Å, c = 18.251(7) Å, alpha = 86.54(4) degrees, beta = 83.17(4) degrees, gamma = 64.14(4) degrees, V = 1280(1) Å(3), space group P&onemacr;, Z = 2, R(1) = 0.071; ArBeSMes(OEt(2)).0.5C(6)H(14) (4.0.5C(6)H(14)), a = 9.732(1) Å, b = 11.190(1) Å, c = 21.841(2) Å, alpha = 75.225(7) degrees, beta = 81.137(8) degrees, gamma = 73.382(8) degrees, V = 2195.3(4) Å(3), space group P&onemacr;, Z = 2, R(1) = 0.062; (ArBeNHPh)(2).C(4)H(10)O (5.C(4)H(10)O), a = 11.894(2) Å, b = 12.212(2) Å, c = 18.709(3) Å, beta = 99.24(1) degrees, V = 2682.4(7) Å(3), space group P2(1), Z = 2, R(1) = 0.045; ArBeNHSiPh(3)(OEt(2)) (6), a = 11.959(2) Å, b = 16.655(2) Å, c = 19.718(2) Å, beta = 105.368(9) degrees, V = 3786.9(8) Å(3), space group P2(1)/c, Z = 4, R(1) = 0.047; ArBeN(SiMe(3))(2) (7), a = 12.623(3) Å, b = 15.404(4) Å, c = 15.502(3) Å, V = 3014(1) Å(3), space group Pbcn, Z = 4, R(1) = 0.046; Ar(THF)(2)Be(OC)(3)Mo(eta(5)-C(5)H(5)).2C(7)H(8) (8.2C(7)H(8)), a = 19.111(4) Å, b = 11.976(3) Å, b = 21.241(5) Å, beta = 103.47(2) degrees, V = 4728(2) Å(3), space group P2(1)/c, Z = 4, R(1) = 0.049; PhC(NSiMe(3))(2)(BeCl)(2)N(SiMe(3))(2) (9), a = 19.996(4) Å, b = 14.816(2) Å, c = 20.183(4) Å, V = 5979(2)Å(3), space group Pbca, Z = 8, R(1) = 0.043; Be{(NSiMe(3))(2)CPh}(2) (10), a = 20.022(2) Å, b = 9.7161(9) Å, c = 19.456(2) Å, beta = 11.392(8) degrees, V = 3524.1(6) Å(3), space group P2(1)/c, Z = 4, R(1) = 0.075.

Journal Article↗
PubMed2006

Ethical considerations in testing workers for the -Glu69 marker of genetic susceptibility to chronic beryllium disease.

OBJECTIVE: The most compelling real-world example of genetic testing for susceptibility to a workplace exposure involves those industries that process or fabricate beryllium. We examined ethical issues associated with testing for susceptibility to chronic beryllium disease. METHODS: Using ethical and clinical criteria, we examined voluntary employer-sponsored testing programs in which individual results are reported directly to workers in a confidential manner. RESULTS: Under reasonable assumptions, the longitudinal positive predictive value of the HLA-DPB1-Glu69 marker of susceptibility to beryllium disease is 12%. Interpretive challenges further limit the utility of the test and may inadvertently suggest a false sense of safety among workers. Concerns about confidential participation and pressures to be tested also must be addressed. CONCLUSIONS: Difficulties surrounding the interpretation of the HLA-DPB1-Glu69 marker, lack of assurance regarding the protection of worker confidentiality, and the potential lowering of social barriers to the implementation of mandatory worker screening combine to make testing beryllium workers inappropriate at this time.

Berylliosis↗
PubMed2006

Chronic beryllium disease and glutathione biosynthesis genes.

OBJECTIVE: Because glutathione (GSH) has been reported to be increased in chronic beryllium disease (CBD) and is associated with immune modulation, associations between CBD and gene polymorphisms of the rate-limiting enzyme in GSH synthesis, glutamate cysteine ligase (GCL), were investigated. Glutamate cysteine ligase consists of a catalytic subunit (GCLC) and modifier subunit (GCLM). METHODS: Patients with CBD, beryllium-sensitized subjects (BeS), and beryllium-exposed subjects without CBD were genotyped for the GCLC GAG trinucleotide repeat polymorphism (GCLC TNR), the GCLC-129 single nucleotide polymorphism (SNP), and the GCLM-588 SNP. RESULTS: Results indicate that GCLC TNR genotype 7/7 is negatively associated with CBD (odds ratio [OR] = 0.28, 95% confidence interval [CI] = 0.08-0.95) and the GCLM-588 C/C SNP genotype is associated with CBD susceptibility (OR = 3.07, 95% CI = 1.00-9.37). No differences were noted in the BeS group. CONCLUSIONS: This study suggests that GSH modulation may play a role in CBD pathogenesis, but not in sensitization to beryllium.

Aged↗
PubMed1994

Beryllium disease: assessment with CT.

PURPOSE: To describe the thin-section computed tomographic (CT) features of beryllium disease and compare the sensitivities of thin-section CT and chest radiography. MATERIALS AND METHODS: In 28 patients with biopsy-proved beryllium disease and 12 healthy control subjects, radiographs were scored with an international classification system. Thin-section CT scans were scored for 11 parenchymal, airway, pleural, and mediastinal findings. RESULTS: Thin-section CT revealed at least one abnormality in 25 patients (89%); chest radiography, in 15 patients (54%). After the finding of bronchial wall thickening attributable to tobacco smoking was excluded, CT scans in 21 (75%) of 28 patients were abnormal because of beryllium disease. The most common CT abnormalities were parenchymal nodules (n = 16) and septal lines (n = 14). With use of CT, abnormalities were detected in 10 (77%) of 13 patients with normal radiographs. CONCLUSION: Thin-section CT was more sensitive than chest radiography in detection of beryllium disease, but the diagnosis was missed in up to 25% of cases with histologic proof.

Berylliosis↗
PubMed1996

Statistical methods for the blood beryllium lymphocyte proliferation test.

The blood beryllium lymphocyte proliferation test (BeLPT) is a modification of the standard lymphocyte proliferation test that is used to identify persons who may have chronic beryllium disease. A major problem in the interpretation of BeLPT test results is outlying data values among the replicate well counts (approximately 7%). A long-linear regression model is used to describe the expected well counts for each set of Be exposure conditions, and the variance of the well counts is proportional to the square of the expected count. Two outlier-resistant regression methods are used to estimate stimulation indices (SIs) and the coefficient of variation. The first approach uses least absolute values (LAV) on the log of the well counts as a method for estimation; the second approach uses a resistant regression version of maximum quasi-likelihood estimation. A major advantage of these resistant methods is that they make it unnecessary to identify and delete outliers. These two new methods for the statistical analysis of the BeLPT data and the current outlier rejection method are applied to 173 BeLPT assays. We strongly recommend the LAV method for routine analysis of the BeLPT. Outliers are important when trying to identify individuals with beryllium hypersensitivity, since these individuals typically have large positive SI values. A new method for identifying large Sls using combined data from the nonexposed group and the beryllium workers is proposed. The log(SI)s are described with a Gaussian distribution with location and scale parameters estimated using resistant methods. This approach is applied to the test data and results are compared with those obtained from the current method.

Berylliosis↗
PubMed2000

Comparative effectiveness of Tiron (4,5-dihydroxy benzene 1,3-disulphonic acid disodium salt) and CaNa2EDTA with time after beryllium poisoning.

The efficacy of two chelating agents (Tiron and calcium disodium EDTA) in the treatment of beryllium induced blood biochemistry and hepatic histopathological alteration was investigated at different duration in female albino rats. Single administration of beryllium nitrate at a dose of 50 mg/kg (im) showed significant decrease in haemoglobin percentage, blood sugar level, protein contents and activity of alkaline phosphatase. On the contrary significant elevation was found in the activity of transaminases (AST and ALT). Tiron was found to be more effective than CaNa2EDTA in reducing the beryllium induced haematological alterations and histopathological lesions in liver. These findings were further confirmed by AAS thus, in which reduced beryllium body burden was seen in liver and blood with Tiron.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗
PubMed1998

[Determination of beryllium in geological samples with slurry sampling and probe atomization in graphite furnace atomic absorption spectrometry].

A method of loading a slurry prepared from a solid sample for analysis of beryllium in geological samples using graphite furnace atomic absorption spectrometry was approached by combining slurry sampling with probe atomization. The factors that influence the performances of beryllium including ashing and atomization temperature, atomization surfaces (probe and tube), the materials of the tube and probe, and the use of matrix modifiers were investigated. The results show that the determination of beryllium in geological samples could be performed by direct slurry sampling with the use of calcium as the matrix modifier for a calibration established with aqueous standards. The relative standard deviations (RSD) of the method were 3.1-5.2%. The analytical results of the geological reference samples were consistent with the certified values. The activation energy during beryllium atomization was calculated using the Arrhenius graph method which was in good with the bonding energy of Be-O.

English Abstract↗
PubMed2005

Chronic beryllium disease: a model for pulmonary sarcoidosis?

Chronic beryllium disease (CBD) and pulmonary sarcoidosis are two distinct chronic disorders, sharing the pathological lung hallmark of the non-caseating granuloma and the immunological feature of T cell activation at the site of disease. However, while CBD is a rare occupational disease in which the cause, i.e. the inhalation of beryllium, is well known since a long time, the etiology of sarcoidosis, which is far more common in the general population, is still unknown. Since granuloma formation requires the presence of an immunogenic initiating antigen, it has been hypothesized that sarcoidosis is an antigen-triggered (auto)immune disease. Furthermore, while the study of large populations exposed to beryllium did made possible the identification of distinct genetic susceptibility factors in CBD, only recently the role of some genetic polymorphisms in sarcoidosis has been unraveled. Therefore, it seems likely that the advancement in the understanding of the immuno-pathogenesis of CBD will also help to design focused genetic studies to finally identify the etiology of sarcoidosis. Moreover, it is also possible that some cases of sarcoidosis are instead been caused by the inhalation of beryllium in genetically susceptible individuals.

Berylliosis↗
PubMedDate not supplied

Beryllium-induced toxicity and its prevention by treatment with chelating agents.

The efficacy of Tiron and calcium disodium EDTA in the treatment of experimental beryllium intoxication was investigated in rats. Beryllium nitrate was administered intramuscularly (50 mg kg(-1)) once only, provoking duration-dependent changes. Maximum changes were recorded after a 7-day regimen. Considerable inhibition was recorded in protein and glycogen contents, as well as in the activity of alkaline phosphatase, glucose-6-phosphatase, acid phosphatase and lipid peroxidation. These parameters were restored considerably with chelation therapy, but comparatively Tiron offered better protection. These findings were further confirmed by atomic adsorption spectrophotometry. Tiron was found to be significantly more effective than CaNa(2)EDTA in reducing the beryllium concentration in the liver, kidney and lungs.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗
PubMed1999

Exposure of cultured murine peritoneal macrophages to low concentrations of beryllium induces increases in intracellular calcium concentrations and stimulates DNA synthesis.

Exposure of humans to beryllium dusts can induce a specific form of chronic pneumonitis that consists mainly of noncaseating granulomas in the lungs. Multiple studies have documented both genetic and immune components of chronic berylliosis. Much work has focused on T cells and their reactivity in berylliosis, but less work has focused on the end effector cells in granulomatous inflammation, macrophages. Because macrophages must become activated to form granulomas, and they become activated by responding to numerous immunomodulatory signals, we investigated the effects of beryllium (BeCl2) on a central signal transduction pathway in macrophages, increases in intracellular calcium ([Ca2+]i). Exposure of cultured murine peritoneal macrophages to low, nontoxic concentrations induced successive spikes or oscillations in [Ca2+]i. Concentrations as low as 5 nM induced significant increases in [Ca2+]i. The source of the increased [Ca2+]i was exclusively extracellular in that increases in [Ca2+]i could be completely blocked by chelating extracellular Ca2+, were inhibited by the Ca2+ channel blocker verapamil, and exposure of macrophages to BeCl2 had no effect on IP3 concentrations. DNA synthesis, a Ca2+-sensitive function, was enhanced in dividing 1LN cells and induced de novo in quiescent macrophages. Furthermore, BeCl2 enhanced DNA synthesis in the absence of coexposure to the protein kinase C activator phorbol myristate acetate. These data support the hypothesis that beryllium toxicity is in part the result of altered Ca2+ metabolism in mononuclear phagocytes consequent to reversible opening of plasma membrane channels.

Animals↗
PubMed1983

Time-lapse cinematographic analysis of beryllium--lung fibroblast interactions.

The proliferative response to beryllium chloride of cells in a population of human lung fibroblasts was quantitatively assessed using time-lapse cinematography. A dose of 0.02 microgram Be/ml, known to decrease the growth rate of fibroblasts, affects an estimated 75% of the cells in the population, increasing their interdivision time (IDT) by approximately 5 hr. The differences in mean 1n(IDT) between treated and control cells were essentially constant for comparable culture sizes ranging from 25 to 250 cells. There was no correlation between mother and daughter cell IDTs in control or treated culture at any culture size. IDTs of sister pairs were highly correlated in control cultures at selected culture sizes while sister pair IDTs of treated cultures were not. The data suggest that while beryllium alters the IDT of fibroblasts, an effect not related to culture size, any given cell affected by beryllium does not impart effects of the mineral to its progeny.

Beryllium↗
PubMed1985

Lung clearance, translocation, and acute toxicity of arsenic, beryllium, cadmium, cobalt, lead, selenium, vanadium, and ytterbium oxides following deposition in rat lung.

Young adult rats were exposed via inhalation or intratracheal instillation to oxides of arsenic, beryllium, cadmium, cobalt, lead, selenium, vanadium, and ytterbium. Serial necropsies were performed to assess the metal content in organs at times up to several weeks after exposure. The lung clearance varied widely for these compounds, and the times to remove 50% of the initial burden ranged from 18 min for vanadium to 400 days for beryllium. Arsenic, cadmium, lead, selenium, and vanadium were initially soluble in lung, but a small fraction (1-20%) remained there over the long term. Extrapulmonary tissues often accumulated substantial amounts of the soluble oxides, and whole-body retention was often greater for compounds that were more soluble in lung. Arsenic, selenium, and vanadium translocated to carcass and bone. Arsenic, cadmium, lead, and selenium accumulated in the liver, and the kidney retained cadmium and lead. Beryllium, cobalt and ytterbium did not deposit at any extrapulmonary site in significant amounts. In general, the aqueous solubility of these compounds was a poor predictor for behavior in vivo because of their interaction with metabolic processes. Of the metal oxides tested for acute lethality following pulmonary deposition, cadmium was most toxic, followed by selenium, vanadium, and arsenic.

Animals↗
PubMed1990

Inhibitory effects of beryllium chloride on rat liver microsomal enzymes.

A single i.v. dose (0.1 mmol Be2+/kg) of beryllium chloride prolonged the duration of pentobarbital-induced sleep and zoxazolamine-induced paralysis, in rats. The effects are correlated with changes of the pharmacokinetic parameters and with the in vitro inhibition of both aliphatic and aromatic hydroxylation of pentobarbital and zoxazolamine. In vitro N-demethylation of meperidine and aminopyrine was partially inhibited while O-demethylation of quinidine was unaffected by liver microsomes of rats pretreated with beryllium salt. The findings give clues that beryllium chloride inhibits some forms of cytochrome P-450, especially those responsible for hydroxylation of substrates, like pentobarbital and zoxazolamine.

Animals↗
PubMed1986

Effect of feeding Gymnema sylvestre leaves on blood glucose in beryllium nitrate treated rats.

The feeding of powdered leaves of Gymnema sylvestre in the diet of rats for 10 days prior and 15 days after i.v. beryllium nitrate significantly protected the animals from the full fall of blood glucose seen in rats receiving beryllium nitrate alone. The feeding of the leaves for 25 days to normal rats did not alter blood glucose significantly. The leaves may contain a principle that could be useful as a prophylactic against beryllium toxicity.

Animals↗
PubMed2005

The structure and the Raman vibrational spectrum of the beryllium aquacation.

The experimental Raman vibrational spectrum of the 5.94 m water solution of the beryllium(II) chloride has been acquired. Theoretical frequencies, infrared and Raman intensities of the vibrational spectrum of the beryllium cation tetrahydrate have been calculated by means of quantum chemical approach. The peaks of the experimental spectrum have been assigned on the basis of the results of the quantum-chemical calculations. It has been shown that the hydrating surrounding of the aquacation increases effectively the frequency of the beryllium-oxygen stretching vibration by 16% in comparison with the free complex.

Beryllium↗
PubMed2000

Determination of beryllium in a stream sediment by high-performance chelation ion chromatography.

High-performance chelation ion chromatography (HPCIC), involving a chelating silica substrate bonded with aminomethylphosphonic acid, has been developed as a novel technique for the quantitative determination of beryllium in complex matrices. An isocratic separation method, using an eluent containing 1 M KNO3, 0.5 M HNO3 and 0.08 M ascorbic acid, allowed the Be2+ to elute away from the sample matrix peak in under 6 min in a sample containing in excess of 800 mg l(-1) matrix metals. A detection limit of 35 microg l(-1) Be(II) was found using a post-column reaction involving Chrome Azurol S (CAS), 1 M hexamine and 10 mM EDTA buffered at pH 6. The standard addition curve gave excellent linearity (R2>0.999). The procedure was applied to the determination of trace beryllium in a certified sediment sample. The results obtained compared well with the certified value for beryllium.

Beryllium↗