Oxidant resistance of cadmium-adapted human lung fibroblasts

Hart, Beth A.; Prabhu, Ramya; Eneman, Jonathan; Durieuxlu, C.C.; Janssen, A. Miranda L.; Borm, Paul J. A.

doi:10.1016/0300-483x(94)02949-u

Cited by 20 publications

(6 citation statements)

References 24 publications

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“…It was therefore hypothesized that Cd resistance might be due to the development of some other permanent protective mechanisms resulting in a gradual decrease of Cd-denatured or otherwise damaged proteins and, consequently, loss of HSP72 overexpression. Among putative mechanisms of protection are those involving metallothioneins (MT), those reinforcing the antioxidant defenses, and those restoring the reduced glutathione (GSH) levels (Hart et al, 1995a(Hart et al, , 1995bHatcher et al, 1995;Shimizu et al, 1997;Gaubin et al, 2000). In our model, the acquired resistance to Cd was found to persist over several weeks of culture even in the absence of the metal.…”

Section: F Croute Et Almentioning

confidence: 81%

Expression of Stress-related Genes in a Cadmium-resistant A549 Human Cell Line

Croute¹,

Beau²,

Murat³

et al. 2005

Journal of Toxicology and Environmental Health, Part A

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This study was designed to explain the basis for Cd-acquired tolerance of A549 cells cultured in the presence of Cd. Thirty-day exposure of cultured human pneumocytes (A549 cell line) to 10 microM Cd was previously found to induce an acquired resistance persisting over several weeks of culture. Moreover, these Cd-resistant cells (R-cells) were found to proliferate faster than controls. No difference was found between R-cells and control cells (S-cells) concerning the basal and Cd-induced level of metallothioneins expression. However, after exposure to Cd, cell glutathione levels were unchanged in R-cells while they were either increased (at 10 microM Cd) or decreased (at 25 microM Cd) in S-cells. cDNA array analysis showed that genes encoding for (GPx1) glutathione peroxidase, glutathione reductase, catalase, and superoxide dismutase were similarly expressed in R- and S-cells, whereas the gene of (GPx2) glutathione peroxidase was overexpressed in R-cells. Most genes encoding stress proteins were similarly expressed, except for HSP27 and GRP94 genes, which were respectively under- (ratio 0.5 +/- 0.1) and over- (1.8 +/- 0.5) expressed in R-cells. Acute exposure to Cd was found to trigger the upregulation of genes encoding the chaperone proteins HSP90A, HSP27, HSP40, GRP78, HSP72, and HO-1 in S-cells. In R-cells, only HO-1 and HSP72 were overexpressed but at a lower level. This suggests that the Cd-related adverse conditions, leading to protein misfolding, are lowered in R-cells. It is likely that the upregulation of GPx2 in R-cells leads to a higher antioxidant defense in these cells.

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Section: F Croute Et Almentioning

confidence: 81%

Expression of Stress-related Genes in a Cadmium-resistant A549 Human Cell Line

Croute¹,

Beau²,

Murat³

et al. 2005

Journal of Toxicology and Environmental Health, Part A

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“…Alveolar epithelial type 2 cells develop resistance to oxidant-induced cytotoxicity after repeated exposure to cadmium aerosols (59). This resistance was also shown in human lung fibroblasts and correlated with increased production of metallothionein, a scavenger of reactive oxygen species (60). Recently, Chambers et al have shown that cadmium salts inhibit fibroblast procollagen production (61) and proteoglycan synthesis (62) in vitro.…”

Section: Cadmiummentioning

confidence: 89%

Inorganic Dust Pneumonias: The Metal-Related Parenchymal Disorders

Kelleher¹,

Pacheco²,

Newman³

2000

Environmental Health Perspectives

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In recent years the greatest progress in our understanding of pneumoconioses, other than those produced by asbestos, silica, and coal, has been in the arena of metal-induced parenchymal lung disorders. Inhalation of metal dusts and fumes can induce a wide range of lung pathology, including airways disorders, cancer, and parenchymal diseases. The emphasis of this update is on parenchymal diseases caused by metal inhalation, including granulomatous disease, giant cell interstitial pneumonitis, chemical pneumonitis, and interstitial fibrosis, among others. The clinical characteristics, epidemiology, and pathogenesis of disorders arising from exposure to aluminum, beryllium, cadmium, cobalt, copper, iron, mercury, and nickel are presented in detail. Metal fume fever, an inhalation fever syndrome attributed to exposure to a number of metals, is also discussed. Advances in our knowledge of antigen-specific immunologic reactions in the lung are particularly evident in disorders secondary to beryllium and nickel exposure, where immunologic mechanisms have been well characterized. For example, current evidence suggests that beryllium acts as an antigen, or hapten, and is presented by antigen-presenting cells to CD4+ T cells, which possess specific surface antigen receptors. Other metals such as cadmium and mercury induce nonspecific damage, probably by initiating production of reactive oxygen species. Additionally, genetic susceptibility markers associated with increased risk have been identified in some metal-related diseases such as chronic beryllium disease and hard metal disease. Future research needs include development of biologic markers of metal-induced immunologic disease, detailed characterization of human exposure, examination of gene alleles that might confer risk, and association of exposure data with that of genetic susceptibility. Key words: aluminum, beryllium, cadmium, cobalt, copper, hard metal disease, iron, mercury, metal fume fever, nickel, pneumoconiosis.-Environ Health Perspect 1 08(suppl 4):685-696 (2000). http.//ehpnetl.niehs.nih.gov/docs/2000/suppl-4/685-696kelleher/abstract.html The term pneumoconiosis, first introduced in the 19th century, refers to diseases and patho-logic consequences from inhalation of particulate dusts. In recent years the greatest progress in our understanding of pneumoconioses, other than those produced by asbestos, silica, and coal, has been in the arena of metal-induced parenchymal lung disorders. As presented in Table 1, various metal dusts and fumes can induce a wide range of lung pathology , including not only parenchymal diseases but airways disorders and cancer as well. In this update we emphasize the parenchymal diseases caused by metal inhalation, including granulomatous disease, giant cell interstitial pneumonitis, chemical pneumonitis, and interstitial fibrosis, among others. Although a number of metals, in addition to those discussed in this chapter, are associated with various forms of lung injury, we have focused this discussion on those for which there has...

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“…Alveolar epithelial type 2 cells develop resistance to oxidant-induced cytotoxicity after repeated exposure to cadmium aerosols (59). This resistance was also shown in human lung fibroblasts and correlated with increased production of metallothionein, a scavenger of reactive oxygen species (60 (85,86). BAL is useful in the diagnosis of lung disorders from hard metals and/or cobalt.…”

Section: Cadmiummentioning

confidence: 99%

Inorganic dust pneumonias: the metal-related parenchymal disorders.

Kelleher

Pacheco

Newman

2000

Environ Health Perspect

150

117

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In recent years the greatest progress in our understanding of pneumoconioses, other than those produced by asbestos, silica, and coal, has been in the arena of metal-induced parenchymal lung disorders. Inhalation of metal dusts and fumes can induce a wide range of lung pathology, including airways disorders, cancer, and parenchymal diseases. The emphasis of this update is on parenchymal diseases caused by metal inhalation, including granulomatous disease, giant cell interstitial pneumonitis, chemical pneumonitis, and interstitial fibrosis, among others. The clinical characteristics, epidemiology, and pathogenesis of disorders arising from exposure to aluminum, beryllium, cadmium, cobalt, copper, iron, mercury, and nickel are presented in detail. Metal fume fever, an inhalation fever syndrome attributed to exposure to a number of metals, is also discussed. Advances in our knowledge of antigen-specific immunologic reactions in the lung are particularly evident in disorders secondary to beryllium and nickel exposure, where immunologic mechanisms have been well characterized. For example, current evidence suggests that beryllium acts as an antigen, or hapten, and is presented by antigen-presenting cells to CD4+ T cells, which possess specific surface antigen receptors. Other metals such as cadmium and mercury induce nonspecific damage, probably by initiating production of reactive oxygen species. Additionally, genetic susceptibility markers associated with increased risk have been identified in some metal-related diseases such as chronic beryllium disease and hard metal disease. Future research needs include development of biologic markers of metal-induced immunologic disease, detailed characterization of human exposure, examination of gene alleles that might confer risk, and association of exposure data with that of genetic susceptibility. Key words: aluminum, beryllium, cadmium, cobalt, copper, hard metal disease, iron, mercury, metal fume fever, nickel, pneumoconiosis. The term pneumoconiosis, first introduced in the 19th century, refers to diseases and pathologic consequences from inhalation of particulate dusts. In recent years the greatest progress in our understanding of pneumoconioses, other than those produced by asbestos, silica, and coal, has been in the arena of metalinduced parenchymal lung disorders. As presented in Table 1 (1). A major theme that emerges in reviewing recent developments in metal-related lung toxicity is the extent to which various metals are capable of inducing both antigen-specific immunologic reactions in the lung and nonspecific "innate" immune system responses characterized by inflammation frequently triggered by oxidant injury. With the recognition of these immune and inflammatory effects comes a growing awareness of the potential hazards to the lung at low levels of exposure. There is also increasing research being conducted on the interaction between metal exposure and the human genome. In the cases of beryllium and cobalt, for example, there is emerging recognition of the spec...

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Oxidant resistance of cadmium-adapted human lung fibroblasts

Cited by 20 publications

References 24 publications

Expression of Stress-related Genes in a Cadmium-resistant A549 Human Cell Line

Expression of Stress-related Genes in a Cadmium-resistant A549 Human Cell Line

Inorganic Dust Pneumonias: The Metal-Related Parenchymal Disorders

Inorganic dust pneumonias: the metal-related parenchymal disorders.

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