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Gill filament permeabilization: A novel approach to assess mitochondrial function in sheepshead minnows (Cyprinodon variegatus) following anthraquinone exposure.
Comparative Biochemistry and Physiology C: Toxicology & Pharmacology ( IF 3.9 ) Pub Date : 2019-12-31 , DOI: 10.1016/j.cbpc.2019.108699
A Reynolds Kirby 1 , Gina Galli 2 , Janna Crossley 1 , Lauren E Sweet 3 , Dane A Crossley 1 , Aaron P Roberts 3
Affiliation  

Anthracene is a highly toxic polycyclic aromatic hydrocarbon (PAH), and its toxicity is increased 8-fold after compounding exposure to UV radiation. Exposure to either the parent or photo-modified compound has been shown to cause increases in reactive oxygen species (ROS) production and lipid peroxidation. Since the majority of ROS production occurs within mitochondria, we investigated simultaneous mitochondrial respiration and ROS production in the gills of sheepshead minnows (Cyprinodon variegatus) acutely (48 h) exposed to anthraquinone (40 μg l-1). Anthraquinone exposure caused a 25% increase in oxidative phosphorylation with electrons donated to Complex I (OXPHOSCI) and a 33% increase in Leak respiration with oligomycin (Leak-OmyCI). ROS production was slightly increased (33.3%) in Leak state with oligomyocin respiring on Complex I substrates (Leak-OmyCI) after anthraquinone exposure, but this value remained unchanged in all other respiratory states. When ROS production was normalized to mitochondrial oxygen consumption, we found that ROS production was decreased in all respiratory states, but most noticeably in the Leak state. We speculate that differences in the antioxidant defense system may have played a role in decreased ROS production. Overall, in this paper we present a novel technique to measure mitochondrial function in the gill filaments of teleost fish exposed to xenobiotic molecules, and we show anthraquinone exposure alters aspects of oxidative phosphorylation and ROS production.

中文翻译:

filament丝通透性:评估蒽醌暴露后羊头min鱼(Cyprinodon variegatus)线粒体功能的新方法。

蒽是一种剧毒的多环芳烃(PAH),复合暴露于紫外线辐射后,其毒性增加了8倍。已经表明,暴露于母体或光改性的化合物会引起活性氧(ROS)产生和脂质过氧化作用的增加。由于大多数ROS的产生都发生在线粒体内,因此我们调查了急性暴露于蒽醌(40μgl-1)的小头head(Cyprinodon variegatus)ill的线粒体呼吸和ROS的同时产生。蒽醌的暴露导致电子复合体I(OXPHOSCI)的电子氧化磷酸化增加25%,而寡霉素(Leak-OmyCI)的泄漏呼吸增加33%。ROS产量略有增加(33。3%)在泄漏状态下,蒽醌暴露后在复合I基质(Leak-OmyCI)上呼吸低聚霉素,但在所有其他呼吸状态下该值均保持不变。当将ROS的产生标准化为线粒体耗氧量时,我们发现ROS的产生在所有呼吸状态下均下降,但在泄漏状态下最为明显。我们推测抗氧化剂防御系统的差异可能在降低ROS产生中发挥了作用。总体而言,在本文中,我们提出了一种新技术来测量暴露于异生物分子的硬骨鱼the线粒体中的线粒体功能,并且我们显示蒽醌暴露会改变氧化磷酸化和ROS产生的方面。当将ROS的产生标准化为线粒体耗氧量时,我们发现ROS的产生在所有呼吸状态下均下降,但在泄漏状态下最为明显。我们推测抗氧化剂防御系统的差异可能在降低ROS产生中发挥了作用。总体而言,在本文中,我们提出了一种新技术来测量暴露于异生物分子的硬骨鱼the线粒体中的线粒体功能,并且我们显示蒽醌暴露会改变氧化磷酸化和ROS产生的方面。当将ROS的产生标准化为线粒体耗氧量时,我们发现ROS的产生在所有呼吸状态下均下降,但在泄漏状态下最为明显。我们推测抗氧化剂防御系统的差异可能在降低ROS产生中发挥了作用。总体而言,在本文中,我们提出了一种新技术来测量暴露于异生物分子的硬骨鱼the线粒体中的线粒体功能,并且我们显示蒽醌暴露会改变氧化磷酸化和ROS产生的方面。
更新日期:2019-12-31
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