Abstract:
Fish in their natural environments possess elaborate mechanisms that regulate physiological function to mitigate the adverse effects of multiple environmental stressors such as temperature, metals, and hypoxia. We investigated how warm acclimation affects mitochondrial responses to Cd, hypoxia, and acute temperature shifts (heat shock and cold snap) in rainbow trout. We observed that state 3 respiration driven by complex I (CI) was resistant to the stressors while warm acclimation and Cd reduced complex I +II (CI + II) driven state 3 respiration. In contrast, state 4 (leak) respirations for both CI and CI + II were consistently stimulated by warm acclimation resulting in reduced mitochondrial coupling efficiency (respiratory control ratio, RCR). Warm acclimation and Cd exacerbated their individual effect on leak respiration to further reduce the RCR. Moreover, the effect of warm acclimation on mitochondrial bioenergetics aligned with its inhibitory effect on activities of citrate synthase and both CI and CII. Unlike the Cd and warm acclimation combined exposure, hypoxia alone and in combination with warm acclimation and/or Cd abolished the stimulation of CI and CI + II powered leak respirations resulting in partial recovery of RCR. The response to acute temperature shifts indicated that while state 3 respiration returned to pre-acclimation level, the leak respiration did not. Overall, our findings suggest a complex in vivo interaction of multiple stressors on mitochondrial function that are not adequately predicted by their individual effects.
摘要:
鱼类在其自然环境中具有复杂的调节生理功能的机制,以减轻多种环境压力的不利影响,如温度,金属,和缺氧。我们研究了温暖的适应如何影响线粒体对Cd的反应,缺氧,和虹鳟鱼的急性温度变化(热休克和寒流)。我们观察到,由复合物I(CI)驱动的状态3呼吸对应激源具有抵抗力,而温暖的适应和Cd减少了复合物III(CIII)驱动的状态3呼吸。相比之下,CI和CI+II的状态4(泄漏)呼吸始终受到温暖适应的刺激,导致线粒体偶联效率降低(呼吸控制比,RCR)。温暖的驯化和Cd加剧了它们对泄漏呼吸的个体影响,从而进一步降低了RCR。此外,热适应对线粒体生物能学的影响与其对柠檬酸合酶和CI和CI活性的抑制作用一致。与Cd和温暖驯化联合暴露不同,单独的缺氧以及与温暖的适应和/或Cd的结合消除了CI和CIII动力的泄漏呼吸的刺激,从而导致RCR的部分恢复。对急性温度变化的反应表明,当状态3呼吸恢复到适应前水平时,泄漏呼吸没有。总的来说,我们的研究结果表明,多种应激源在线粒体功能上存在复杂的体内相互作用,但它们的个体效应不能充分预测.