Authors: | Tierney, K; Casselman, M; Takeda, S; Farrell, T; Kennedy, C |
Year: | 2007 |
Journal: | Environmental Toxicology and Chemistry 26: 998-1004 |
Title: | The relationship between cholinesterase inhibition and two types of swimming performance in chlorpyrifos-exposed coho salmon (Oncorhynchus kisutch) |
Abstract: | Brain acetylcholinesterase (AChE) activity was evaluated after two different swimming tests in coho salmon (Oncorhynchus kisutch; 238 +/- 5 g) given 96-h exposures to 0, 5, 10, 20, or 40 mu g/L of chlorpyrifos. Brain AChE activity decreased in a concentration-dependent manner (AChE activities were 81.8, 52.2, 37.3, and 21.3% of control for the 5, 10, 20, and 40 mu g/L exposures, respectively), whereas swimming performance was impaired after a threshold of AChE impairment was reached. Specifically, for swimming performance (U-crit measured using the established ramp-U-crit test (duration, 152 +/- 8 min), this threshold occurred with AChE activity of 68.5% +/- 18.1% of control. For a rapid acceleration test (U-Delta V, where V represents velocity; 27.6 +/- 0.8 min), this value was 52.6% +/- 15.4% of control. Both swim protocols resulted in similar maximum swim speeds (control ramp-U-crit and U-Delta V values of 3.44 +/- 0.09 and 3.71 +/- 0.13 body lengths/s, respectively), and performance was significantly reduced after 20 and 40 mu g/L exposures in both groups (ramp-U-crit values: 86.4 and 83.6%, respectively, of control; U-Delta V values: 85.2 and 77.8%, rsepectively, of control). Although both tests yielded similar swim speeds, postexercise plasma lactate concentrations were greater for the U-Delta V test (11.3 +/- 0.6 vs 8.6 +/- 0.5 mmol/L), indicating a greater anaerobic effort. This increase was exaggerated after 10 mu g/L of chlorpyrifos (14.6 +/- 1.3 mmol/L), indicating that anaerobic muscle was used to attain the same speed. Given the threshold relationship between AChE inhibition and swimming performance, coho salmon appear able to maintain integrated swimming activity despite significant impairment of an underlying neurological control mechanism. |
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