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1.
J Appl Toxicol ; 44(9): 1403-1415, 2024 Sep.
Article de Anglais | MEDLINE | ID: mdl-38778435

RÉSUMÉ

Beryllium sulfate (BeSO4) can cause inflammation through the mechanism, which has not been elucidated. Mitochondrial DNA (mtDNA) is a key contributor of inflammation. With mitochondrial damage, released mtDNA can bind to specific receptors (e.g., cGAS) and then activate related pathway to promote inflammatory responses. To investigate the mechanism of mtDNA in BeSO4-induced inflammatory response in 16HBE cells, we established the BeSO4-induced 16HBE cell inflammation model and the ethidium bromide (EB)-induced ρ016HBE cell model to detect the mtDNA content, oxidative stress-related markers, mitochondrial membrane potential, the expression of the cGAS-STING pathway, and inflammation-related factors. Our results showed that BeSO4 caused oxidative stress, decline of mitochondrial membrane potential, and the release of mtDNA into the cytoplasm of 16HBE cells. In addition, BeSO4 induced inflammation in 16HBE cells by activating the cGAS-STING pathway. Furthermore, mtDNA deletion inhibited the expression of cGAS-STING pathway, IL-10, TNF-α, and IFN-ß. This study revealed a novel mechanism of BeSO4-induced inflammation in 16HBE cells, which contributes to the understanding of the molecular mechanism of beryllium and its compounds-induced toxicity.


Sujet(s)
Béryllium , ADN mitochondrial , Inflammation , Protéines membranaires , Nucleotidyltransferases , Transduction du signal , Humains , ADN mitochondrial/effets des médicaments et des substances chimiques , ADN mitochondrial/métabolisme , Nucleotidyltransferases/métabolisme , Nucleotidyltransferases/génétique , Protéines membranaires/métabolisme , Protéines membranaires/génétique , Inflammation/induit chimiquement , Inflammation/métabolisme , Béryllium/toxicité , Transduction du signal/effets des médicaments et des substances chimiques , Lignée cellulaire , Stress oxydatif/effets des médicaments et des substances chimiques , Potentiel de membrane mitochondriale/effets des médicaments et des substances chimiques
4.
J Trace Elem Med Biol ; 76: 127125, 2023 Mar.
Article de Anglais | MEDLINE | ID: mdl-36623420

RÉSUMÉ

PURPOSE: Beryllium is known to have adverse health effects and is classified as carcinogenic to humans. However, data on systemic beryllium exposure in humans are rare and especially human toxicokinetics are largely uncharted. As such, the first reported multi-annual course of blood and urine concentrations after a high exposure scenario provides important new insights. METHODS: For a medical follow-up biomonitoring samples were collected for 56 months from a male subject after an accidental and multi-faceted high exposure. Sampling started on day 2 post-exposure for urine and day 147 for blood. The samples were analyzed by inductively coupled mass spectrometry (ICP-MS) and plotted longitudinally as a function of time. Terminal half-lives were calculated assuming a first-order elimination process. MAIN FINDINGS: Both matrices showed highly increased initial concentrations (about 100-fold), despite the 147-day delay in blood sampling, and a marked decline over time. In urine, a two-phase excretion process was suspected based on the longitudinal data. Calculations gave terminal half-lives of 117.5 days and 666.5 days for phases 1 and 2, respectively. Blood kinetics called for a terminal half-life of 103.5 days. Elimination kinetics in blood and urine were comparable, simultaneously gathered samples showed an excellent correlation (R² = 0.985). PRINCIPAL CONCLUSIONS: The long-term follow-up after a high initial exposure to beryllium provides the first detailed insights into the elimination course of systemically available beryllium in humans. Conform kinetics of beryllium in urine and blood and the strong correlation between both parameters indicate high data validity and support the good representation of the current systemically available beryllium by urine and blood concentration in humans. The relatively long terminal half-lives in both matrices suggest a possible accumulation in humans in case of repeated exposures.


Sujet(s)
Béryllium , Surveillance biologique , Humains , Mâle , Béryllium/toxicité , Béryllium/urine , Toxicocinétique , Spectrométrie de masse/méthodes
5.
Toxicol Appl Pharmacol ; 449: 116097, 2022 08 15.
Article de Anglais | MEDLINE | ID: mdl-35679967

RÉSUMÉ

Beryllium and its compounds can cause pulmonary interstitial fibrosis through mechanisms that are not yet clear. Long non-coding RNA (lncRNA) is implicated in various diseases. The molecular toxicity of beryllium sulfate (BeSO4) was investigated through the RNA-seq analysis of the lncRNA and mRNA whole-transcriptome of BeSO4-treated 16HBE cells. A total of 1014 lncRNAs (535 upregulated and 479 downregulated) and 4035 mRNAs (2224 upregulated and 1811 downregulated) were found to be significantly dysregulated (|logFC| ≥> 2.0, p < 0.05) in the BeSO4-treated groups when compared with the control group. Five differentially expressed lncRNAs and mRNAs were verified by qRT-PCR. KEGG analysis showed that lncRNA regulates the ECM receiver interaction and PI3K/AKT signaling pathways, etc. In addition, H19:17, lnc-C5orf13-1:1, lnc-CRYAA-17:1, lnc-VSTM5-1:11, and lnc-THSD7A-7:1 may regulate BeSO4-induced 16HBE cytotoxicity through ceRNA mechanism. The results of this study will provide some theoretical support for the study of the toxic mechanism of beryllium and its compounds.


Sujet(s)
ARN long non codant , Béryllium/toxicité , Analyse de profil d'expression de gènes/méthodes , Réseaux de régulation génique , Phosphatidylinositol 3-kinases/métabolisme , ARN long non codant/génétique , ARN long non codant/métabolisme , ARN messager/génétique , ARN messager/métabolisme , Transcriptome
6.
Toxicol Lett ; 361: 64-71, 2022 May 15.
Article de Anglais | MEDLINE | ID: mdl-35427767

RÉSUMÉ

Dermal exposure to hazardous substances such as chemicals, toxics, metallic items and other contaminants may present substantial danger for health. Beryllium (Be) is a hazardous metal, especially when inhaled and/or in direct contact with the skin, associated with chronic beryllium disease (CBD) and Be sensitization (BeS). The objective of this study was to investigate the percutaneous penetration of beryllium and copper contained in metallic items as eyeglass temple tips (specifically BrushCAST® Copper Beryllium Casting Alloys containing Be 0.35 < 2.85%; Cu 95.3-98.7%), using Franz diffusion cells. This work demonstrated that the total skin absorption of Cu was higher (8.86%) compared to Be (4.89%), which was expected based on the high percentage of Cu contained in the eyeglass temple tips. However, Be accumulated significantly in the epidermis and dermis (up to 0.461 µg/cm2) and, to a lesser extent, in the stratum corneum (up to 0.130 µg/cm2) with a flux of permeation of 3.52 ± 4.5 µg/cm2/hour and lag time of 2.3 ± 1.3 h, after cutaneous exposure of temple tip into 1.0 mL artificial sweat for 24 h. Our study highlights the importance of avoiding the use of Be alloys in items following long-term skin contact.


Sujet(s)
Bérylliose , Béryllium , Alliages , Béryllium/toxicité , Cuivre/toxicité , Lunettes correctrices , Humains
7.
J Appl Toxicol ; 42(9): 1524-1532, 2022 Sep.
Article de Anglais | MEDLINE | ID: mdl-35289950

RÉSUMÉ

Inhalation of beryllium and its compounds can cause lung injuries, resulting from inflammation and oxidative stress. Multivesicular bodies (MVB), such as exosomes, are membrane vesicles produced by early and late endosomes that mediate intercellular communications. However, the role of exosomes in beryllium toxicity has not been elucidated. This current study aimed to investigate the functional role of exosomes in lung injury resulting from beryllium sulfate (BeSO4 ). Here, Sprague-Dawley (SD) rats were exposed to 4, 8, and 12 mg/kg BeSO4 by nonexposed intratracheal instillation. Murine macrophage (RAW 264.7) cells were pretreated with 50 nmol/L rapamycin (an mTOR signaling pathway inhibitor) for 30 min and then cultured for 24 h with 100 µg/mL exosomes, which had been previously isolated from the serum of 12 mg/kg BeSO4 -treated SD rats. Compared with those of the controls, exposure to BeSO4 in vivo increased LDH activity, elevated levels of inflammatory cytokines (IL-10, TNF-α, and IFN-γ) alongside inflammation-related proteins expression (COX-2 and iNOS), and enhanced secretion of exosomes from the SD rat's serum. Moreover, the BeSO4 -Exos-induced upregulation of LDH activity and inflammatory responses in RAW 264.7 cells can be alleviated following pretreatment with rapamycin. Collectively, these results suggest that serum exosomes play an important role in pulmonary inflammation induced by BeSO4 in RAW 264.7 cells via the mTOR pathway.


Sujet(s)
Béryllium , Exosomes , Animaux , Béryllium/pharmacologie , Béryllium/toxicité , Exosomes/métabolisme , Inflammation/induit chimiquement , Macrophages , Souris , Rats , Rat Sprague-Dawley , Sirolimus/métabolisme , Sérine-thréonine kinases TOR/métabolisme
8.
Occup Environ Med ; 79(2): 120-126, 2022 02.
Article de Anglais | MEDLINE | ID: mdl-34535537

RÉSUMÉ

OBJECTIVES: Human leukocyte antigen-DP beta 1 (HLA-DPB1) with a glutamic acid at the 69th position of the ß chain (E69) genotype and inhalational beryllium exposure individually contribute to risk of chronic beryllium disease (CBD) and beryllium sensitisation (BeS) in exposed individuals. This retrospective nested case-control study assessed the contribution of genetics and exposure in the development of BeS and CBD. METHODS: Workers with BeS (n=444), CBD (n=449) and beryllium-exposed controls (n=890) were enrolled from studies conducted at nuclear weapons and primary beryllium manufacturing facilities. Lifetime-average beryllium exposure estimates were based on workers' job questionnaires and historical and industrial hygienist exposure estimates, blinded to genotype and case status. Genotyping was performed using sequence-specific primer-PCR. Logistic regression models were developed allowing for over-dispersion, adjusting for workforce, race, sex and ethnicity. RESULTS: Having no E69 alleles was associated with lower odds of both CBD and BeS; every additional E69 allele increased odds for CBD and BeS. Increasing exposure was associated with lower odds of BeS. CBD was not associated with exposure as compared to controls, yet the per cent of individuals with CBD versus BeS increased with increasing exposure. No evidence of a gene-by-exposure interaction was found for CBD or BeS. CONCLUSIONS: Risk of CBD increases with E69 allele frequency and increasing exposure, although no gene by environment interaction was found. A decreased risk of BeS with increasing exposure and lack of exposure response in CBD cases may be due to the limitations of reconstructed exposure estimates. Although reducing exposure may not prevent BeS, it may reduce CBD and the associated health effects, especially in those carrying E69 alleles.


Sujet(s)
Bérylliose/génétique , Béryllium/toxicité , Chaines bêta des antigènes HLA-DP/génétique , Exposition professionnelle/effets indésirables , Bérylliose/épidémiologie , Études cas-témoins , Maladie chronique , Femelle , Génotype , Humains , Mâle , Polymorphisme génétique , Études rétrospectives
9.
J Hazard Mater ; 421: 126757, 2022 01 05.
Article de Anglais | MEDLINE | ID: mdl-34352522

RÉSUMÉ

Inhalation exposure and beryllium (Be) toxicity are well-known, but research on bioaccessibility from soils via different exposure pathways is limited. This study examined soils from a legacy radioactive waste disposal site using in vitro ingestion (Solubility Bioaccessibility Research Consortium [SBRC], physiologically based extraction test [PBET], in vitro gastrointestinal [IVG]), inhalation (simulated epithelial lung fluid [SELF]) and dynamic two-stage bioaccessibility (TBAc) methods, as well as 0.43 M HNO3 extraction. The results showed, 70 ±â€¯4.8%, 56 ±â€¯16.8% and 58 ±â€¯5.7% of total Be were extracted (gastric phase [GP] + intestinal phase [IP]) in the SBRC, PBET, and IVG methods, respectively. Similar bioaccessibility of Be (~18%) in PBET-IP and SELF was due to chelating agents in the extractant. Moreover, TBAc-IP showed higher extraction (20.8 ±â€¯2.0%) in comparison with the single-phase (SBRC-IP) result (4.8 ±â€¯0.23%), suggesting increased Be bioaccessibility and toxicity in the gastrointestinal tract when the contamination derives from the inhalation route. The results suggested Be bioaccessibility depends on solution pH; time of extraction; soil reactive fractions (organic-inorganic); particle size, and the presence of chelating agents in the fluid. This study has significance for understanding Be bioaccessibility via different exposure routes and the application of risk-based management of Be-contaminated sites.


Sujet(s)
Arsenic , Polluants du sol , Arsenic/analyse , Béryllium/toxicité , Biodisponibilité , Pollution de l'environnement , Sol , Polluants du sol/analyse , Polluants du sol/toxicité
10.
J Appl Toxicol ; 42(2): 230-243, 2022 02.
Article de Anglais | MEDLINE | ID: mdl-34091916

RÉSUMÉ

Beryllium and its compounds are systemic toxicants that are widely applied in many industries. Hydrogen sulfide has been found to protect cells. The present study aimed to determine the protective mechanisms involved in hydrogen sulfide treatment of 16HBE cells following beryllium sulfate-induced injury. 16HBE cells were treated with beryllium sulfate doses ranging between 0 and 300 µM BeSO4 . Additionally, 16HBE cells were subjected to pretreatment with either a 300 µM dose of sodium hydrosulfide (a hydrogen sulfide donor) or 10 mM DL-propargylglycine (a cystathionine-γ-lyase inhibitor) for 6 hr before then being treated with 150 µM beryllium sulfate for 48 hr. This study illustrates that beryllium sulfate induces a reduction in cell viability, increases lactate dehydrogenase (LDH) release, and increases cellular apoptosis and autophagy in 16HBE cells. Interestingly, pretreating 16HBE cells with sodium hydrosulfide significantly reduced the beryllium sulfate-induced apoptosis and autophagy. Moreover, it increased the mitochondrial membrane potential and alleviated the G2/M-phase cell cycle arrest. However, pretreatment with 10 mM DL-propargylglycine promoted the opposite effects. PI3K/Akt/mTOR and Nrf2/ARE signaling pathways are also activated following pretreatment with sodium hydrosulfide. These results indicate the protection provided by hydrogen sulfide in 16HBE cells against beryllium sulfate-induced injury is associated with the inhibition of apoptosis and autophagy through the activation of the PI3K/Akt/mTOR and Nrf2/ARE signaling pathways. Therefore, hydrogen sulfide has the potential to be a promising candidate in the treatment against beryllium disease.


Sujet(s)
Apoptose/effets des médicaments et des substances chimiques , Autophagie/effets des médicaments et des substances chimiques , Béryllium/toxicité , Sulfure d'hydrogène/pharmacologie , Agents protecteurs/pharmacologie , Bronches , Lignée cellulaire , Cellules épithéliales , Humains
13.
J Clin Invest ; 131(9)2021 05 03.
Article de Anglais | MEDLINE | ID: mdl-33630763

RÉSUMÉ

Discovering dominant epitopes for T cells, particularly CD4+ T cells, in human immune-mediated diseases remains a significant challenge. Here, we used bronchoalveolar lavage (BAL) cells from HLA-DP2-expressing patients with chronic beryllium disease (CBD), a debilitating granulomatous lung disorder characterized by accumulations of beryllium-specific (Be-specific) CD4+ T cells in the lung. We discovered lung-resident CD4+ T cells that expressed a disease-specific public CDR3ß T cell receptor motif and were specific to Be-modified self-peptides derived from C-C motif ligand 4 (CCL4) and CCL3. HLA-DP2-CCL/Be tetramer staining confirmed that these chemokine-derived peptides represented major antigenic targets in CBD. Furthermore, Be induced CCL3 and CCL4 secretion in the lungs of mice and humans. In a murine model of CBD, the addition of LPS to Be oxide exposure enhanced CCL4 and CCL3 secretion in the lung and significantly increased the number and percentage of CD4+ T cells specific for the HLA-DP2-CCL/Be epitope. Thus, we demonstrate a direct link between Be-induced innate production of chemokines and the development of a robust adaptive immune response to those same chemokines presented as Be-modified self-peptides, creating a cycle of innate and adaptive immune activation.


Sujet(s)
Bérylliose/immunologie , Béryllium/toxicité , Lymphocytes T CD4+/immunologie , Chimiokine CCL3/immunologie , Chimiokine CCL4/immunologie , Poumon/immunologie , Animaux , Antigènes , Bérylliose/génétique , Bérylliose/anatomopathologie , Lymphocytes T CD4+/anatomopathologie , Chimiokine CCL3/génétique , Chimiokine CCL4/génétique , Maladie chronique , Femelle , Chaines bêta des antigènes HLA-DP/génétique , Chaines bêta des antigènes HLA-DP/immunologie , Humains , Immunité innée/effets des médicaments et des substances chimiques , Immunité innée/génétique , Poumon/anatomopathologie , Mâle , Souris
14.
Chest ; 159(3): 1084-1093, 2021 03.
Article de Anglais | MEDLINE | ID: mdl-32926872

RÉSUMÉ

BACKGROUND: Chronic beryllium disease (CBD), a granulomatous disease with similarities to sarcoidosis, arises only in individuals exposed to beryllium. Inhaled beryllium can elicit a T-cell-dominated alveolitis leading nonnecrotizing granulomata. CBD can be distinguished from sarcoidosis by demonstrating beryllium sensitization in a lymphocyte proliferation test. RESEARCH QUESTION: Beryllium exposure usually occurs in an occupational setting. Because of the diagnosis of CBD in a patient without evident beryllium exposure, we performed a beryllium-lymphocyte proliferation test (BeLPT) among his work colleagues. STUDY DESIGN AND METHODS: This field study investigated a cohort of work colleagues without obvious beryllium exposure. Twenty-one of 30 individuals were assessed in our outpatient clinic for beryllium sensitization. Therefore, BeLPT was performed with freshly collected peripheral blood mononuclear cells. Data were extracted from clinical charts, including geographical data. Beryllium content in dust samples collected at the workplace was measured by graphite-furnace atomic absorption spectroscopy and was compared with samples from different areas of Germany. RESULTS: For the initial patient, the diagnosis of sarcoidosis was reclassified as CBD based on two positive BeLPT results. Assessment of his workplace did not identify a source of beryllium. However, BeLPTs performed on his workmates demonstrated beryllium sensitization in 5 of 21 individuals, suggesting a local beryllium source. Concrete dust obtained from the building yard, the workplace of the index patient, contained high amounts of beryllium (1138 ± 162 µg/kg), whereas dust from other localities (control samples) showed much lower beryllium content (range, 147 ± 18-452 ± 206 µg/kg). Notably, the control dust collected from different places all over Germany exhibit different beryllium concentrations. INTERPRETATION: We describe a cluster of beryllium-sensitized workers from an industry not related to beryllium caused by environmental exposure to beryllium-containing concrete dust, which exhibited markedly elevated beryllium content. Importantly, analyses of dust samples collected from different localities showed that they contain markedly different amounts of beryllium. Thus, besides workplace-related exposure, environmental factors also are capable of eliciting a beryllium sensitization.


Sujet(s)
Bérylliose , Béryllium , Poussière/analyse , Exposition environnementale , Granulome de l'appareil respiratoire , Activation des lymphocytes/immunologie , Sarcoïdose pulmonaire/diagnostic , Adulte , Bérylliose/diagnostic , Bérylliose/étiologie , Bérylliose/immunologie , Bérylliose/prévention et contrôle , Béryllium/analyse , Béryllium/toxicité , Industrie de la construction , Diagnostic différentiel , Exposition environnementale/effets indésirables , Exposition environnementale/analyse , Femelle , Allemagne/épidémiologie , Granulome de l'appareil respiratoire/induit chimiquement , Granulome de l'appareil respiratoire/diagnostic , Humains , Tests immunologiques/méthodes , Agranulocytes , Mâle , Agrégat spatio-temporel , Lieu de travail/normes
15.
J Appl Toxicol ; 41(8): 1275-1285, 2021 08.
Article de Anglais | MEDLINE | ID: mdl-33197057

RÉSUMÉ

Beryllium and its compounds are systemic toxicants that mainly accumulate in the lungs. As a regulator of gene expression, microRNAs (miRNAs) were involved in some lung diseases. This study aimed to analyze the levels of some inflammatory cytokine and the differential expressions of miRNAs in human bronchial epithelial cells (16HBE) induced by beryllium sulfate (BeSO4 ) and to further explore the biological functions of differentially expressed miRNAs. The profile of miRNAs in 16HBE cells was detected using the high-throughput sequencing between the control groups (n = 3) and the 150 µmol/L of BeSO4 -treated groups (n = 3). Bioinformatics analysis of differentially expressed miRNAs was performed, including the prediction of target genes, Gene Ontology (GO) analysis, and the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to verify some damage-related miRNAs. We found that BeSO4 can increase the levels of some inflammatory cytokine such as interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α), interferon-γ (IFN-γ), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). And BeSO4 altered miRNAs expression of 16HBE cells and a total of 179 differentially expressed miRNAs were identified, including 88 upregulated miRNAs and 91 downregulated miRNAs. The target genes predicted by 28 dysregulated miRNAs were mainly involved in the transcription regulation, signal transduction, MAPK, and VEGF signaling pathway. The qRT-PCR verification results were consistent with the sequencing results. miRNA expression profiling in 16HBE cells exposed to BeSO4 provides new insights into the toxicity mechanism of beryllium exposure.


Sujet(s)
Béryllium/toxicité , Bronches/effets des médicaments et des substances chimiques , microARN/métabolisme , Muqueuse respiratoire/effets des médicaments et des substances chimiques , Transcriptome/effets des médicaments et des substances chimiques , Technique de Western , Bronches/cytologie , Bronches/métabolisme , Lignée cellulaire , Survie cellulaire/effets des médicaments et des substances chimiques , Cytokines/métabolisme , Test ELISA , Séquençage nucléotidique à haut débit , Humains , Réaction de polymérisation en chaine en temps réel , Muqueuse respiratoire/cytologie , Muqueuse respiratoire/métabolisme
16.
Medicina (Kaunas) ; 56(11)2020 Nov 22.
Article de Anglais | MEDLINE | ID: mdl-33266389

RÉSUMÉ

Background: Chronic beryllium disease (CBD) is a granulomatous disease that resembles sarcoidosis but is caused by beryllium. Clinical manifestations similar to those observed in CBD have occasionally been reported in exposure to dusts of other metals. However, reports describing the clinical, radiographic, and pathological findings in conditions other than beryllium-induced granulomatous lung diseases, and detailed information on mineralogical analyses of metal dusts, are limited. Case presentation: A 51-year-old Japanese man with rapidly progressing nodular shadows on chest radiography, and a 10-year occupation history of underground construction without beryllium exposure, was referred to our hospital. High-resolution computed tomography showed well-defined multiple centrilobular and perilobular nodules, and thickening of the intralobular septa in the middle and lower zones of both lungs. No extrathoracic manifestations were observed. Pathologically, the lung specimens showed 5-12 mm nodules with dust deposition and several non-necrotizing granulomas along the lymphatic routes. X-ray analytical electron microscopy of the same specimens revealed aluminum, iron, titanium, and silica deposition in the lung tissues. The patient stopped smoking and changed his occupation to avoid further dust exposure; the chest radiography shadows decreased 5 years later. Conclusion: The radiological appearances of CBD and sarcoidosis are similar, although mediastinal or hilar lymphadenopathy is less common in CBD and is usually seen in the presence of parenchymal opacities. Extrathoracic manifestations are also rare. Despite limited evidence, these findings are similar to those observed in pneumoconiosis with a sarcoid-like reaction due to exposure to dust other than of beryllium. Aluminum is frequently detected in patients with pneumoconiosis with a sarcoid-like reaction and is listed as an inorganic agent in the etiology of sarcoidosis. It was also detected in our patient and may have contributed to the etiology. Additionally, our case suggests that cessation of dust exposure may contribute to improvement under the aforementioned conditions.


Sujet(s)
Bérylliose , Pneumoconiose , Sarcoïdose , Bérylliose/imagerie diagnostique , Béryllium/toxicité , Poussière , Humains , Mâle , Adulte d'âge moyen , Pneumoconiose/imagerie diagnostique , Pneumoconiose/étiologie , Sarcoïdose/imagerie diagnostique
17.
J Occup Environ Med ; 62(1): 64-73, 2020 01.
Article de Anglais | MEDLINE | ID: mdl-31743304

RÉSUMÉ

OBJECTIVE: To evaluate interaction of HLA-DPß1 and DRß1 polymorphisms with metrics of beryllium exposure, in the development of beryllium sensitization (BeS) and chronic beryllium disease (CBD). METHODS: A matched case-control study of 61 CBD, 41 BeS, and 259 controls from two beryllium-processing facilities. RESULTS: BES and CBD were significantly associated with presence of DPßE69. Dose response of exposure was not observed for the development of BES and CBD with/without adjustment for DPßE69 (P > 0.05). The DRßE71 polymorphism was more common in BeS than CBD after adjusting for exposure and maybe a protective factor (aOR 0.4, 95% CI 0.2 to 0.9) against the progression of BeS to CBD. CONCLUSION: No exposure-response association was found, which may reflect that the workers in this high exposure cohort were above a threshold level where an exposure-response could be observed.


Sujet(s)
Bérylliose/génétique , Béryllium/toxicité , Exposition professionnelle/statistiques et données numériques , Études cas-témoins , Études de cohortes , Chaines bêta des antigènes HLA-DP/génétique , Humains , Protéines de tissu nerveux/génétique , Polymorphisme génétique , Protéines de liaison à l'ARN/génétique
19.
Exp Lung Res ; 45(3-4): 92-100, 2019.
Article de Anglais | MEDLINE | ID: mdl-31155972

RÉSUMÉ

Objective: We aimed to determine whether beryllium toxicity was associated with mitochondria apoptosis pathway in SD rats. Methods: Thirty-two SD rats were given an intratracheal instillation dose of 10 g/l beryllium oxide (0.5 ml per rat). Additional 32 rats were given an intratracheal instillation dose of 0.9% normal saline (0.5 ml per rat). The percentage of apoptosis, mitochondrial membrane potential, the expression level of apoptosis related genes and proteins, including bcl2, Bax and Caspase-3 were detected. Results: The average of percentage of apoptosis, the expression of caspase-3, bax, and cytochrome c were decreased significantly in lung tissues from rats exposed to beryllium oxide compared to normal controls. The expression of bcl2 and ADP were increased significantly at 80 d after exposure. Conclusions: We conclude that inhibition of apoptosis by beryllium oxide involves mitochondrial apoptosis pathway in rat model of beryllium oxide-induced pulmonary disease.


Sujet(s)
Apoptose/effets des médicaments et des substances chimiques , Béryllium/toxicité , Maladies pulmonaires/anatomopathologie , Mitochondries/métabolisme , ADP/métabolisme , Animaux , Caspase-3/métabolisme , Cytochromes c/métabolisme , Maladies pulmonaires/induit chimiquement , Protéines proto-oncogènes c-bcl-2/métabolisme , Rats
20.
Plant Physiol Biochem ; 139: 691-696, 2019 Jun.
Article de Anglais | MEDLINE | ID: mdl-31054471

RÉSUMÉ

Industrialization and inevitable mining has resulted in the release of some metals in environments, which have numerous industrial roles on one hand and also showed environmental toxicity on other hand. Beryllium is one of them, it has been used in number of industries however its excess use or inappropriate disposal of beryllium resulted in high beryllium accumulation in soil and ground water. This subsequently is affecting our environment and more potentially arable crop production. Beryllium has been extensively studied in humans and reported as toxic metal. In plants, only few studies have been documented toxic effects of beryllium in plants. Moreover, plant products (fruits, grains or other plant parts) could be major source of beryllium toxicity in our food chain therefore it is more imperative to understand how plant can be developed more tolerant to beryllium toxicity. In this short mini-review article, we primarily highlighted and speculated different beryllium uptake, translocation and beryllium storage mechanism in plants. This article provides considerable information for people who are working in identifying and developing heavy metal hyper accumulators plants.


Sujet(s)
Béryllium/métabolisme , Béryllium/toxicité , Plantes/métabolisme , Dépollution biologique de l'environnement , Pollution de l'environnement/prévention et contrôle , Plantes/effets des médicaments et des substances chimiques
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