Environmental arsenic exposure and sputum metalloproteinase concentrations

Josyula, Arun B.; Poplin, Gerald S.; Kurzius-Spencer, Margaret; McClellen, Hannah E.; Kopplin, Michael J.; Stürup, Stefan; Lantz, R. Clark; Burgess, Jefferey L.

doi:10.1016/j.envres.2006.01.003

Cited by 37 publications

(45 citation statements)

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“…We have shown that mice chronically exposed to 10 -50 ppb arsenic in drinking water increase mRNA for MMP-9 and a battery of proteins consistent with alterations in cell migration (26), as well as for altered bronchiolar lavage proteins (27) that included a biomarker for reduced wound healing [receptor for advanced glycation end products (RAGE)]. We have additionally reported that low-dose arsenic exposure (ϳ20 ppb) in drinking water results in changes in specific wound repair proteins (e.g., RAGE and the MMP-9/TIMP-1 ratio) recovered from human sputum (23,27). The work reported herein helps clarify initial cellular changes in human lung epithelial cells that, albeit on a more acute and at slightly higher concentrations than reported in the animal and human studies, may contribute to low-dose arsenic effects in the lung.…”

Section: Discussionmentioning

confidence: 92%

“…We have recently begun to evaluate the effects of chronic, low-dose arsenic (i.e., Ͻ100 ppb) exposure on lung tissue using protein and mRNA analyses from mouse models (26,27) and sputum analyses from human populations (23,27). Combined findings from these studies suggested that ingestion of arsenic may alter wound response and specifically, MMP-9/TIMP-1 ratios in the lung (23,26,27). In this report, we used acute arsenic exposure with an in vitro human cell model in an attempt to directly examine potential cellular mechanisms of arsenic exposure in the lung epithelium.…”

Section: Discussionmentioning

confidence: 99%

“…Because in vivo biomarker data suggested that chronic arsenic exposure altered cell migrations and wound repair in the lung (23,26,27), we examined whether arsenic had an acute effect on wound healing of human airway epithelial cells in culture. In these experiments, 16HBE14o-cells were grown without arsenic until confluence.…”

Section: Arsenic Slows Wound Repair Of Human Airway Epithelial Cells mentioning

confidence: 99%

“…Additional microarray experiments on lung tissue from mice fed low-dose arsenic revealed several changes in extracellular matrix (ECM) protein expression and a large increase in matrix metalloproteinase (MMP)-9 expression (26). In human studies for low-level arsenic exposure lung biomarkers, we found an increase in the ratio of MMP-9 to tissue inhibitor of matrix metalloproteinase (TIMP)-1 in collected sputum samples (23). MMPs are responsible for ECM degradation among other proteolyses.…”

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confidence: 91%

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Arsenic upregulates MMP-9 and inhibits wound repair in human airway epithelial cells

Olsen

Liguori

Zong

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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As part of the innate immune defense, the polarized conducting lung epithelium acts as a barrier to keep particulates carried in respiration from underlying tissue. Arsenic is a metalloid toxicant that can affect the lung via inhalation or ingestion. We have recently shown that chronic exposure of mice or humans to arsenic (10-50 ppb) in drinking water alters bronchiolar lavage or sputum proteins consistent with reduced epithelial cell migration and wound repair in the airway. In this report, we used an in vitro model to examine effects of acute exposure of arsenic (15-290 ppb) on conducting airway lung epithelium. We found that arsenic at concentrations as low as 30 ppb inhibits reformation of the epithelial monolayer following scrape wounds of monolayer cultures. In an effort to understand functional contributions to epithelial wound repair altered by arsenic, we showed that acute arsenic exposure increases activity and expression of matrix metalloproteinase (MMP)-9, an important protease in lung function. Furthermore, inhibition of MMP-9 in arsenic-treated cells improved wound repair. We propose that arsenic in the airway can alter the airway epithelial barrier by restricting proper wound repair in part through the upregulation of MMP-9 by lung epithelial cells.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Arsenic Slows Wound Repair Of Human Airway Epithelial Cells mentioning

confidence: 99%

mentioning

confidence: 91%

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Arsenic upregulates MMP-9 and inhibits wound repair in human airway epithelial cells

Olsen

Liguori

Zong

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…High dosage of orpiment ensures good therapeutic effect though it involves severe side-effects and arsenic has been considered as a poisonous cocarcinogen for some human malignancies, especially for skin and lung cancer. [4][5][6][7][8][9] Therefore, it is extremely important to improve its bioavailability and curative effect and reduce its dosage and side effects by changing the form of orpiment.…”

Section: Introductionmentioning

confidence: 99%

Preparation of Orpiment Nanoparticles and Their Cytotoxic Effect on Cultured Leukemia K562 Cells

Lin

Wang²,

Zhang³

2007

j nanosci nanotechnol

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An investigation has been made into the antitumor effect on K562 cells of orpiment nanoparticles which were prepared chemically and analyzed by transmission electron microscope and energy dispersive spectrometry (EDS). Methyl thiazolyl tetrazolium and flow cytometry assays were performed to examine their antitumor effect compared with that of traditional orpiment at various concentrations. The average diameters of the two types of orpiment nanoparticles prepared were 60 nm and 140 nm, respectively, and EDS identified that only orpiment was present. Orpiment nanoparticles greatly inhibited the proliferation of K562 cells by apoptosis, in a concentration-and time-dependent manner, much more effectively than traditional orpiment (p < 0.001). The survival ratio of cells treated with orpiment nanoparticles at 2, 4, 8, and 16 micromol/l after 72 h was 23.0%, 10.1%, 3.2%, and 0.5%, respectively, much lower than 80.0%, 69.0%, 52.3%, and 31.7% of cells treated with traditional orpiment at the corresponding concentration for 72 h. The IC50 of orpiment nanoparticles in K562 cells for 48 h was only 1.27 micromol/l, in comparison with 13.0 micromol/l of traditional orpiment. After treated with orpiment nanoparticles at 4, 8, and 16 micromol/l for 48 h, the apoptotic rate of cells was 11.55%, 20.70%, and 26.45%, respectively, but that in cells treated with traditional orpiment at the same concentration for 48 h was only 3.16%, 3.86%, and 6.46%, respectively. Thus, orpiment nanoparticles can produce a much better cytotoxic effect on cancer cells than that of traditional orpiment.

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Lung Cancer and Other Pulmonary Diseases

Sherwood

Lantz

2015

Arsenic

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Environmental arsenic exposure and sputum metalloproteinase concentrations

Cited by 37 publications

References 46 publications

Arsenic upregulates MMP-9 and inhibits wound repair in human airway epithelial cells

Arsenic upregulates MMP-9 and inhibits wound repair in human airway epithelial cells

Preparation of Orpiment Nanoparticles and Their Cytotoxic Effect on Cultured Leukemia K562 Cells

Lung Cancer and Other Pulmonary Diseases

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