Author(s): McKenzie DJ, Shingles A, Claireaux G, Domenici P
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Abstract The fast-start escape response in fish is essential for predator avoidance, but almost nothing is known about whether sublethal concentrations of pollutants can impair this reflex. Ammonia, a pervasive pollutant of aquatic habitats, is known to have toxic effects on nervous and muscle function in teleost fish. Golden gray mullet (Liza aurata L.) were exposed for 24 h to sublethal ammonia concentrations in seawater (control, 400 micromol L(-1), or 1,600 micromol L(-1) NH(4)Cl), and then their response to startling with a mechanical stimulus was measured with high-speed video. Initiation of the escape response was significantly slowed by ammonia exposure: response latency rose proportionally from <50 ms in controls to >300 ms at a concentration of 1,600 micromol L(-1 ) NH(4)Cl. This indicates toxic effects on nervous function within the reflex arc. Impaired escape performance was also observed: maximum turning rate, distance covered, velocity, and acceleration were significantly reduced by >45\% at a concentration of 1,600 micromol L(-1) NH(4)Cl. This indicates toxic effects on fast-twitch glycolytic white muscle function, the muscle type that powers the fast-start response. These neuromotor impairments were associated with significant ammonia accumulations in venous plasma and white muscle and brain tissue. These results indicate that anthropogenic ammonia pollution in aquatic habitats may increase the vulnerability of fish to predation, especially by birds and mammals that are not affected by water ammonia concentrations.
This article was published in Physiol Biochem Zool
and referenced in Journal of Bioremediation & Biodegradation