|Abstract or Summary
- Sablefish, Anoplopoma fimbria, is a valuable North Pacific Ocean species caught in several commercial fisheries and is often discarded due to size or catch limits. Managers must account for the mortality of discarded fish to assess fish populations and harvest impacts, yet discard mortality rates of specific fisheries are generally unknown. Delayed mortality is one source of undetected mortality in discarded fish. The observance of delayed mortality in discards during laboratory and field studies suggest that capture stressors may induce physiological modifications that result indirectly in future mortality from stress and/or disease. Since the imposition of a stressor disrupts a fish's capability to maintain immunological function, understanding the capacity of the immune system to function after an acute bycatch stressor may be important in assessing the survival of discarded fish and further understanding the mechanisms behind delayed mortality. The main objective of this study was to describe the immunological health of sablefish exposed to capture stressors. First, experiments were performed to obtain the
conditions necessary for [³H]-thymidine incorporation into lymphocytes sensitive to B and T cell mitogens. Then, in laboratory experiments designed to simulate the capture process, sablefish were subjected to various stressors that may influence survival: towing in a net, hooking, ecologically relevant temperatures of seawater and air, and air exposure time. Following the imposition of stress, the immunological assay was used to assess immune function. The results demonstrated that regardless of fishing gear type, exposure to elevated seawater temperatures or air times, [³H]-thymidine incorporation into leukocytes from stressed sablefish was significantly diminished in response to the T cell mitogen concanavalin A or the B cell mitogen lipopolysaccharide. Seawater or air temperatures were not found to significantly influence immune responses. The duration and severity of the capture stressors applied in our study were sufficient to induce significantly elevated levels of cortisol and glucose. However, there was no difference in the magnitude of plasma cortisol and glucose responses among stress treatments. These data suggest that immunological suppression occurs in sablefish subjected to capture-related
stressors. Functional impairment of the immune system after exposure to capture-related stress is a potential reason for delayed mortality in discarded sablefish. As fishes are returned to the ocean, their ability to perform at the whole organism level may be diminished for an extended period of time and the cumulative strain from maintaining physiological adaptation can reduce their ability to sustain normal immunological functions. Consequently, immunological impairment may predispose a discarded fish to disease and eventual death. However, further studies are needed to determine if delayed mortality in discarded sablefish can be caused by increased susceptibility to infectious agents resulting from stress-mediated immunosuppression.