Toxicity of metallic ions and oxides to rabbit alveolar macrophages

Labedzka, Maria; Gulyas, Holger; Schmidt, Norbert; Gercken, G.

doi:10.1016/s0013-9351(89)80039-8

Cited by 45 publications

(14 citation statements)

References 20 publications

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“…As a possible factor responsible for this inhibitory effect, multiple but common metal contents might be operative. Indeed, in addition to arsenic, cadmium (mostly present in CU particles), vanadium (mostly present in FA particles), and zinc (present in both particulates), in the form of ions and oxides, can affect the ability of A M to release important mediators (Labedzka et al, 1989;Geertz et al, 1994). Depression of reactive oxygen species released by A M exposed to mineral dusts has been attributed to their heavy metal contents (Gulyas & Gercken, 1988;Gulyas et al, 1990), and i t has been suggested that these modifications could be responsible for the enhanced susceptibility to bacterial and viral infections of animals exposed to arsenic (Hatch et al, 1981;Aranyi et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

Reduction of the Ex Vivo Production of Tumor Necrosis Factor Alpha by Alveolar Phagocytes After Administration of Coal Fly Ash and Copper Smelter Dust

Broeckaert

Buchet

Huaux

et al. 1997

Journal of Toxicology and Environmental Health

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We investigated the effect of intratracheally instilled coal fly ash (FA) and copper smelter dust (CU) on the lung integrity and on the ex vivo release of tumor necrosis factor alpha (TNF-alpha) by alveolar phagocytes. Groups of female NMRI mice received a single intratracheal administration of different particles normalized for the arsenic content (20 micrograms/kg body weight, i.e., 600 ng arsenic/mouse) and the particle load (100 mg/kg body weight, i.e., 3 mg/mouse). Mice received tungsten carbide (WC) alone (100 mg/kg), FA alone (100 mg/kg, i.e., 20 micrograms arsenic/kg), CU mixed with WC (CU, 13.6 mg/kg, i.e., 20 micrograms arsenic/kg; WC, 86.4 mg/kg) and Ca3(AsO4)2 mixed with WC (20 micrograms arsenic/kg; WC, 100 mg/kg). Animals were sacrificed at 1, 6, or 30 d posttreatment and analyzed by bronchoalveolar lavage for total protein (TP) content, inflammatory cell number and type, and TNF-alpha production. Additional mice were studied to evaluate particle retention by measuring total arsenic retention in the lung at appropriate times. Instillation of WC induced a mild and transient (d 1) inflammatory reaction characterized by an increase of TP and an influx of polymorphonuclear leukocytes in the alveolar compartment. Compared to WC, Ca3(AsO4)2 produced a significant increase of TP content in BALF. CU particles caused a severe but transient inflammatory reaction, while a persisting alveolitis (30 d) was observed after treatment with FA. Compared to control saline, a marked inhibition of TNF-alpha release was observed in response to LPS in all groups at d 1. Cytokine production was upregulated in WC- and Ca3(AsO4)1-treated animals after 6 and 30 d, respectively. However, a 90% inhibition of TNF-alpha production was still observed at d 30 after administration of CU and FA. Although arsenic was cleared from the lung tissue 6 d after Ca3(AsO4)2 administration, a significant fraction persisted (10-15% of the arsenic administered) in the lung of CU- and FA-treated mice at d 30. We hypothetize that suppression of TNF-alpha production is dependent upon the slow elimination of the particles and their metal content from the lung.

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Section: Discussionmentioning

confidence: 99%

Reduction of the Ex Vivo Production of Tumor Necrosis Factor Alpha by Alveolar Phagocytes After Administration of Coal Fly Ash and Copper Smelter Dust

Broeckaert

Buchet

Huaux

et al. 1997

Journal of Toxicology and Environmental Health

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“…Apart from obvious species differences, solubility differences between V 2 O 5 and NH4VO3 might have contributed to these discrepancies. Variable effects upon biological responses as a function of metal solubility (and subsequent variations in bioavailability) are well known for several transition metals (Waters et al, 1974;Labedzka et al, 1989;Zelikoff and Cohen, 1995;Cohen et al, 1996a).…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Immunotoxicity of Inhaled Ammonium Metavanadate in Fisher 344 Rats

et al. 1996

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Male Fisher 344 rats were exposed to 2 mg vanadium(V)/m 3 (as ammonium metavanadate NFL,VO 3 , 0.32 ^m MMD) atmospheres for 8 hr/day for 4 days in a nose-only exposure system. In exposed rats, lung V burdens increased in a time-dependent fashion. Analysis of lung cells and lavage fluid 24 hr after the final exposure suggested that tissue damage and a strong inflammatory response was elicited; numbers of neutrophil and small macrophages (Me), as well as levels of lavageable protein and lactate dehydrogenase, were significantly elevated as compared with levels observed with air-exposed rats. Vanadium also affected pulmonary alveolar M0 (PAM) capacities to produce and respond to immunoregulating cytokines. Inducible PAM production of tumor necrosis factor-a was significantly Inhibited, as was the ability to increase cell surface Class II/I-A molecule expression in response to interferon-? (LFN-)'). PAM from V-exposed hosts were also inhibited in their ability to be primed by EFN-y to produce superoride anion and hydrogen peroxide in response to stimulation with opsonized zymosan. These studies indicate that short-term repeated exposure of rats to atmospheric V, at levels encountered in an occupational setting, can alter host pulmonary immunomocompetence, with one major effect occurring at the level of cytokine-related functions. These alterations may be underlying mechanisms for the welldocumented increases in bronchopulmonary infections and cancers in workers chronically exposed to V-containing atmospheres.O 1996 Society of Toxicology.Vanadium (V), a Group Vb transition metal, is used widely in the steel and chemical industries, and is a constituent of many ores, coals, and oils (ATSDR, 1991). Increased mining and milling of V-bearing ores and combustion of fossil fuels for heating/energy production result in high levels of respirable V particles/fumes (containing both insoluble vanadium pentoxide and soluble vanadates) in many work environs (Nriagu and Pacyna, 1988; ATSDR, 1991). Ambient V levels in these settings can reach >30 mg/m 3 ; the ' To whom correspondence should be addressed. Fax: (914) 351-5472.

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“…Subchronic and/or acute exposure of various rodent hosts to V v induced: decreased alveolar macrophage (AM) phagocytosis and lysosomal enzyme activity and release (36,37,38,39); altered lung immune cell population numbers and profiles (40,41,42,43); modified mast cell histamine release (44); increased in situ (but not in vitro) AM expression/production of MIP-2 and KC CXC chemokine mRNA (45); and, airway fibrosis (46,47). This latter study also reported a similar effect when vanadyl sulfate (VOS0 4 ) was used, suggesting that some aspects of the pulmonary immunotoxicity of V may not be valence-dependent.…”

Section: Effects Of Vanadium On the Lungs And Their Immune System-assmentioning

confidence: 99%

“…As noted earlier, these likely included differential effects on production of IL-1, TNFa, and IFNy (39,42,67), as well as of select chemokines (i.e., MIP-2 and KC [45]) critical to inflammatory cell recruitment during the antibacterial response. Solubility-based differential effects on phagocytic function (4,38,68,117) also likely affected how rats responded to Listeria. If AM only displayed reduced phagocytic function, increased amounts of Listeria would stay extracellular and need to be ingested and killed by any still func tional AM.…”

Section: Role Of Physicochemical Properties In Pulmonary Immunotoxicomentioning

confidence: 99%

Toxicity of Vanadium Compounds: Pulmonary and Immune System Targets

Cohen

2007

Vanadium: The Versatile Metal

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Inhalation is the most prevalent route of human exposure to insoluble pentavalent vanadium(V) oxides and soluble salts in urban/occupational settings. While initial pulmonary clearance of both soluble and insoluble forms of V is fairly rapid, complete clearance/degree of absorption of any V agent is ultimately a function of its solubility. Nevertheless, there are still several general toxicologic outcomes that arise from lung deposition of various V agents (as pure compounds or Vcontaminated dusts). Workers exposed to V-bearing dusts or fumes display an increased incidence of several lung diseases (e.g., asthma, bronchitis, pneumonia). Similarly, after deposi tion of urban particulate matter (PM) or residual oil fly ash (ROFA), animals develop states of immunomodulation (inflammation, neutrophilic alveolitis, modified resistance to infection) that correlate with the levels of V in the particles. This presentation focused on how general (and in some cases agent-specific) mechanisms have been formulated to explain how entrained V agents induce toxicity and immunomodula tion in the lungs.

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Toxicity of metallic ions and oxides to rabbit alveolar macrophages

Cited by 45 publications

References 20 publications

Reduction of the Ex Vivo Production of Tumor Necrosis Factor Alpha by Alveolar Phagocytes After Administration of Coal Fly Ash and Copper Smelter Dust

Reduction of the Ex Vivo Production of Tumor Necrosis Factor Alpha by Alveolar Phagocytes After Administration of Coal Fly Ash and Copper Smelter Dust

Pulmonary Immunotoxicity of Inhaled Ammonium Metavanadate in Fisher 344 Rats

Toxicity of Vanadium Compounds: Pulmonary and Immune System Targets

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