Onukwufor John O, Kamunde Collins
Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY 14642, USA; Department of Biomedical Sciences, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, PE C1A 4P3, Canada.
Department of Biomedical Sciences, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, PE C1A 4P3, Canada.
Ecotoxicol Environ Saf. 2025 Jan 1;289:117450. doi: 10.1016/j.ecoenv.2024.117450. Epub 2024 Dec 3.
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.
生活在自然环境中的鱼类拥有复杂的机制来调节生理功能，以减轻多种环境应激源（如温度、金属和缺氧）的不利影响。我们研究了暖适应如何影响虹鳟鱼线粒体对镉、缺氧和急性温度变化（热休克和寒潮）的反应。我们观察到，由复合体I（CI）驱动的状态3呼吸对这些应激源具有抗性，而暖适应和镉会降低由复合体I + II（CI + II）驱动的状态3呼吸。相反，暖适应持续刺激CI和CI + II的状态4（基础）呼吸，导致线粒体偶联效率（呼吸控制率[RCR]）降低。暖适应和镉加剧了它们对基础呼吸的个体影响，进一步降低了RCR。此外，暖适应对线粒体生物能量学的影响与其对柠檬酸合酶以及CI和CII活性的抑制作用一致。与镉和暖适应的联合暴露不同，单独的缺氧以及与暖适应和/或镉的联合作用消除了对CI和CI + II驱动的基础呼吸的刺激，导致RCR部分恢复。对急性温度变化的反应表明，虽然状态3呼吸恢复到适应前水平，但基础呼吸没有。总体而言，我们的研究结果表明，多种应激源在线粒体内存在复杂的体内相互作用，其个体效应无法充分预测这种相互作用。
