Enhanced superoxide anion production in activated peritoneal macrophages from English sole (Pleuronectes vetulus) exposed to PACs
- NMFS/NOAA, Seattle, WA (United States)
In fish, as in mammals, macrophages play a vital role in the destruction of infective organisms. The purpose of this study was to determine if peritoneal macrophages (M{O}s) from English sole (Pleuronectes vetulus), a marine benthic fish, have an altered ability to produce cytotoxic reactive oxygen intermediates (ROIs) after exposure to polycyclic aromatic compounds (PACs). ROIs are the principle product of M{O}s used to destroy engulfed organisms. Assay conditions, including the concentration of M{O}s, type of in vitro stimulant, tissue culture media, and incubation time were optimized to measure the production of superoxide anion (O{sub 2}{minus}), the progenitor ROI, in English sole M{O}s. English sole were injected with an organic solvent extract of a PAH-contaminated sediment, equivalent to 20g sediment/kg fish, via their dorsal lymphatic sinus, and peritoneal M{O}s were harvested on days 1, 3, 5, 7, and 14 post injection. Activated peritoneal M{O}s from English sole injected with the sediment extract produced significantly more superoxide radicals after stimulation in vitro with either opsonized zymosan (OZ) or phorbol myristate acetate (PMA) than the vehicle injected or control fish. Specifically, activated peritoneal M{O}s stimulated with PMA in vitro produced greater amounts (compared to controls) of O{sub 2}{minus} on days 7 and 14 after exposure, whereas the same cells stimulated with OZ showed heightened production only on day 7 after exposure. No differences in the basal amounts of O{sub 2}{minus} production from activated peritoneal M{O}s between the treatment groups were observed. This study shows that exposure of English sole to PACs altered production of O{sub 2}{minus} by macrophages, however, the consequence to the immunocompetence of exposed fish remains to be elucidated.
- OSTI ID:
- 244872
- Report Number(s):
- CONF-9511137--; ISBN 1-880611-03-1
- Country of Publication:
- United States
- Language:
- English
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