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The physiological consequences of exposure to chronic, sublethal waterborne nickel in rainbow trout (Oncorhynchus mykiss): exercisevsresting physiology
Author(s) -
Eric F. Pane,
Aziz Haque,
Greg G. Goss,
Chris M. Wood
Publication year - 2004
Publication title -
journal of experimental biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.367
H-Index - 185
eISSN - 1477-9145
pISSN - 0022-0949
DOI - 10.1242/jeb.00871
Subject(s) - rainbow trout , gill , acclimatization , respiratory system , biology , medicine , physiology , osmoregulation , endocrinology , zoology , chemistry , anatomy , ecology , fish <actinopterygii> , fishery , salinity
In rainbow trout (Oncorhynchus mykiss), following chronic (42 day) exposure to both 384 microg Ni l(-1) and 2034 microg Ni l(-1), Ni accumulation was greatest in the gill, kidney and plasma, with the plasma as the main sink for Ni. Indeed, trapped plasma analysis revealed that extensive loading of Ni in the plasma accounted for substantial percentages of accumulated Ni in several tissues including the liver and heart. Accumulated Ni in the gill and kidney was less dependent on plasma Ni concentration, suggesting a more intracellular accumulation of Ni in these tissues. We present evidence for a clear, persistent cost of acclimation to chronic, sublethal Ni exposure. Chronic (40-99 day) exposure to sublethal waterborne Ni (243-394 microg Ni l(-1); approximately 1% of the 96 h LC(50)) impaired the exercise physiology, but not the resting physiology, of rainbow trout. Ni acted as a limiting stressor, decreasing maximal rates of oxygen consumption (MO2,max) during strenuous exercise in trout exposed for 34 days to sublethal Ni. This drop in high-performance gas exchange was attributed mainly to a reduction in relative branchial diffusing capacity (D(rel)) caused by thickening of secondary lamellae. Morphometric analysis of the gills of chronically exposed fish revealed overall swelling of secondary lamellae, as well as hypertrophic respiratory epithelia within secondary lamellae. Additionally, contraction of the lamellar blood pillar system and narrowing of interlamellar water channels occurred, possibly contributing to decreased high-performance gas exchange. Decreased aerobic capacity persisted in fish previously exposed to nickel despite a clean-water exposure period of 38 days and an almost complete depuration of gill Ni, suggesting that extrabranchial mechanisms of chronic Ni toxicity may also be important. Chronic impairment of such a dynamically active and critical organ as the gill may depress the overall fitness of a fish by impairing predator avoidance, prey capture and migration success with obvious environmental implications.

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