Beaumont M W, Butler P J, Taylor E W
School of Biosciences, The University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
J Exp Biol. 2003 Jan;206(Pt 1):153-62. doi: 10.1242/jeb.00060.
The present study was undertaken to answer two questions relating to the exposure of brown trout Salmo trutta to sublethal concentrations of copper and low pH (CLP) for 96 h. (1) What is the effect of these pollutants on the rate of oxygen consumption (M(O(2))) at different levels of exercise and (2) why does ammonia accumulate within these fish, when the low external pH should favour the diffusion of NH(3) across the gills? Mean M(O(2)) of fish in CLP and control (normal pH and no added copper) conditions were not significantly different from each other at any level of exercise. This suggests that exposure to CLP was not a 'loading' factor at any level of activity. However, both maximum M(O(2)) and critical swimming speed (U(crit)) were significantly lower in the CLP trout (5.5+/-1.6 mmol O(2) kg(-1) h(-1) and 1.12+/-0.06 BL s(-1), respectively) than in control fish (18.5+/-2.3 mmol O(2) kg(-1) h(-1) and 2.04+/-0.11 BL s(-1), respectively). There was no evidence from cardiovascular variables, such as heart rate and cardiac output, to suggest any changes in the oxygen transport system to compensate for any possible reduction in branchial gas exchange. Thus, it is suggested that oxygen exchange and transport do not limit the swimming performance of CLP trout, but that exposure to CLP reduces the maximum demand for O(2), i.e. it is a limiting factor. The accumulation of ammonia in the plasma and white muscles during exposure to CLP has already been implicated in reducing the swimming performance of brown trout. Inhibition of cortisol synthesis abolished a large proportion of the increases in both the accumulation and excretion of ammonia that occurred during the second 48 h of the exposure to CLP, but did not inhibit ammonia accumulation completely. It is suggested that CLP not only causes an increase in the rate of production of ammonia, which is enhanced when the level of cortisol starts to increase after 48 h, but that it also inhibits an excretory mechanism (most probably Na(+)/NH(4)(+) exchange) that is non-obligatory under 'normal' conditions (when passive diffusion is sufficient), but is required in order to respond to unusually high ammonia loads.
本研究旨在回答与褐鳟(Salmo trutta)在亚致死浓度的铜和低pH值(CLP)环境中暴露96小时相关的两个问题。(1)这些污染物在不同运动水平下对耗氧率(M(O₂))有何影响,以及(2)当外部低pH值应有利于NH₃通过鳃扩散时,为什么这些鱼体内会积累氨?在任何运动水平下,处于CLP环境和对照(正常pH值且未添加铜)条件下的鱼的平均M(O₂)彼此之间均无显著差异。这表明在任何活动水平下,暴露于CLP都不是一个“负荷”因素。然而,CLP环境中的褐鳟的最大M(O₂)和临界游泳速度(U(crit))(分别为5.5±1.6 mmol O₂ kg⁻¹ h⁻¹和1.12±0.06 BL s⁻¹)均显著低于对照鱼(分别为18.5±2.3 mmol O₂ kg⁻¹ h⁻¹和2.04±0.11 BL s⁻¹)。没有证据表明心血管变量(如心率和心输出量)有任何变化,以表明氧运输系统有任何改变来补偿鳃气体交换可能出现的任何减少。因此,有人认为氧交换和运输并不限制CLP环境中褐鳟的游泳性能,但暴露于CLP会降低对O₂的最大需求,即它是一个限制因素。在暴露于CLP期间,血浆和白色肌肉中氨的积累已被认为与褐鳟游泳性能的降低有关。皮质醇合成的抑制消除了在暴露于CLP的第二个48小时期间氨积累和排泄增加的很大一部分,但并未完全抑制氨的积累。有人认为,CLP不仅会导致氨生成速率增加,当48小时后皮质醇水平开始升高时这种增加会加剧,而且它还会抑制一种排泄机制(很可能是Na⁺/NH₄⁺交换),这种机制在“正常”条件下(当被动扩散足够时)是非必需的,但在应对异常高的氨负荷时是必需的。