Effect of arsenic exposure on alveolar macrophage function. I. Effect of soluble As(III) and As(V)

Robert Clark Lantz, G. Parliman, Jie Chen Guan Jie Chen, D. E. Carter

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Abstract

Despite potential differences in the mechanism and potency of toxicity between the two common oxidation states of arsenic (As(III) and As(V)), assessments of the risk from inhaled arsenic generally ignore the oxidation state of inorganic arsenicals. Differences between potency and toxicity of As(III) and As(V) were evaluated by determining alteration in function of pulmonary alveolar macrophages (PAM) following in vivo and in vitro exposure to soluble arsenic. Male Sprague-Dawley rats were used throughout. One day following intratracheal instillation of 1 mg/ml (as arsenic) of either sodium arsenite (As(III)) or sodium arsenate (As(V)), PAM were lavaged and analyzed for alterations in superoxide (O2-), prostaglandin E2 (PGE2), and tumor necrosis factor (TNF-α) production. There were no differences in bronchoalveolar lavage fluid PGE2 or TNF-α. PAM lavaged from As(V)-exposed animals showed significant increases in O2- production. In vivo exposure to either oxidative form of arsenic decreased basal and lipopolysaccharide (LPS)-induced release of TNF-α production by PAM, but did not suppress LPS- induced production of PGE2. To test the direct effects of arsenic on PAM function, PAM were lavaged from control animals and exposed, in vitro, to either arsenical for up to 24 hr to concentrations of 0.1 to 300 μg/ml arsenic. Doses used were not cytotoxic to PAM, since LDH release was not significantly increased, even at the highest dose. Significant dose-dependent inhibition of O2- production was only evident after 24 hr exposure to arsenicals. As(III) was more potent than As(V), inhibiting O2- at concentrations as low as 0.1 μg/ml compared to 1.0 μg/ml of As(V). Suppression of LPS-induced release of TNF-α also occurred at lower concentrations of As(III), 50% inhibition at 0.15 μg/ml, compared to As(V), 50% inhibition at 1.8 μg/ml. While As(III) exposure had no affect on PGE2 production, As(V) caused inhibition of LPS-induced PGE2 production at concentrations above 1.0 μg/ml. Differences between As(III) and As(V) indicate that different mechanisms and/or potencies exist between the two arsenic species. Arsenic-induced alteration in PAM function may compromise host defense against infections and alter immune surveillance.

Original languageEnglish (US)
Pages (from-to)183-195
Number of pages13
JournalEnvironmental Research
Volume67
Issue number2
DOIs
StatePublished - 1994

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Alveolar Macrophages
Arsenic
arsenic
Dinoprostone
Arsenicals
tumor
Lipopolysaccharides
Tumor Necrosis Factor-alpha
Toxicity
Animals
sodium
toxicity
exposure
effect
oxidation
Oxidation
arsenite
animal
arsenate
Superoxides

ASJC Scopus subject areas

  • Environmental Science(all)

Cite this

Effect of arsenic exposure on alveolar macrophage function. I. Effect of soluble As(III) and As(V). / Lantz, Robert Clark; Parliman, G.; Guan Jie Chen, Jie Chen; Carter, D. E.

In: Environmental Research, Vol. 67, No. 2, 1994, p. 183-195.

Research output: Contribution to journalArticle

Lantz, Robert Clark ; Parliman, G. ; Guan Jie Chen, Jie Chen ; Carter, D. E. / Effect of arsenic exposure on alveolar macrophage function. I. Effect of soluble As(III) and As(V). In: Environmental Research. 1994 ; Vol. 67, No. 2. pp. 183-195.
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