Metal-induced modulation of nitric oxide production in vitro by murine macrophages: Lead, nickel, and cobalt utilize different mechanisms

Tian, L; Lawrence, DA

HERO ID

84260

Reference Type

Journal Article

Year

1996

Language

English

PMID

8975779

HERO ID 84260
In Press No
Year 1996
Title Metal-induced modulation of nitric oxide production in vitro by murine macrophages: Lead, nickel, and cobalt utilize different mechanisms
Authors Tian, L; Lawrence, DA
Journal Toxicology and Applied Pharmacology
Volume 141
Issue 2
Page Numbers 540-547
Abstract Macrophages (M phi) can be induced to produce nitric oxide (NO), which has been suggested to be important for macrophages to exercise various functions. We have previously reported that an environmental toxicant, lead (Pb), can significantly inhibit NO production by murine splenic M phis. Herein, eight additional metal ions, gold (Au), cadmium (Cd), cobalt (Co), chromium (Cr), copper (Cu), mercury (Hg), nickel (Ni), and zinc (Zn), were assessed. In addition to Pb, Hg and Cd significantly suppressed NO production by cytokine (interferon-gamma and tumor necrosis factor-alpha)-stimulated murine M phis. Au and Cu also were inhibitory, but less than Pb, Hg, and Cd. In contrast, Cr and Zn were not modulatory, and Ni and Co significantly enhanced NO production by cytokine-stimulated M phis. The enhancement by Ni and Co was inhibited by the arginine analog N-monomethylarginine. The metals showed different activating/inhibiting profiles when added to a cell-free (activated M phi lysate) NO-producing-system in which inducible NO synthase (iNOS) is already expressed. Cr, Cu, Pb, and Zn moderately suppressed iNOS, which suggests that they may directly modify enzyme or cofactor activity. Cd, Hg, Mg, Ni, or Co did not produce any significant effect on NO production by the cell-free system. Inhibition of NO production by Pb-exposed M phis was not due to decreased expression of iNOS nor limited to its modest direct inhibition of iNOS; thus, other mechanism(s) must be accountable for the efficient Pb-induced inhibition of NO production by M phi. Ni or Co did induce a substantial increase of iNOS protein. Overall, these observations provide additional insight into the means by which metals via inhibition or enhancement of NO production may be pathogenic, by suppression of defense mechanisms or induction of hypersensitivity, respectively.
Doi 10.1006/taap.1996.0320
Pmid 8975779
Wosid WOS:A1996WC22200022
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English