Fisheries Behavioral Ecology - Abstracts
Lupes, S.C., M.W. Davis, B.L. Olla,
and C.B. Schreck. 2006. Capture-related stressors impair immune system
function in sablefish. Transactions of the American Fisheries Society 135:129-138.
Abstract
The sablefish Anoplopoma fimbria is a valuable North Pacific Ocean species that, when not
targeted in various commercial fisheries, is often a part of discarded bycatch. Predictions of the survival of
discarded fish are dependent on understanding how a fish responds to stressful conditions. Our objective was
to describe the immunological health of sablefish exposed to capture stressors. In laboratory experiments
designed to simulate the capture process, we subjected sablefish to various stressors that might influence
survival: towing in a net, hooking, elevated seawater and air temperatures, and air exposure time. After stress
was imposed, the in vitro mitogen-stimulated proliferation of sablefish leukocytes was used to evaluate the
function of the immune system in an assay we validated for this species. The results demonstrated that
regardless of fishing gear type, exposure to elevated seawater temperature, or time in air, the leukocytes from
stressed sablefish exhibited significantly diminished proliferative responses to the T-cell mitogen, concanavalin A, or the B-cell mitogen, lipopolysaccharide. There was no difference in the immunological
responses associated with seawater or air temperature. The duration and severity of the capture stressors
applied in our study were harsh enough to induce significantly elevated levels of plasma cortisol and glucose,
but there was no difference in the magnitude of levels among stressor treatments. These data suggest that
immunological suppression occurs in sablefish subjected to capture-related stressors. The functional
impairment of the immune system after capture presents a potential reason why delayed mortality is possible
in discarded sablefish. Further studies are needed to determine whether delayed mortality in discarded
sablefish can be caused by increased susceptibility to infectious agents resulting from stressor-mediated
immunosuppression.
Last updated
26 April, 2007
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