Laboratory of Animal Physiology, Department of Zoology, Faculty of Sciences, School of Biology, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Department of Animal Science, Faculty of Agricultural Sciences, University of Western Macedonia, Florina, Greece.
Am J Physiol Regul Integr Comp Physiol. 2020 Sep 1;319(3):R264-R281. doi: 10.1152/ajpregu.00066.2020. Epub 2020 Jul 1.
Long-term exposure of to temperatures beyond 26°C triggers mussel mortality. The present study aimed to integratively illustrate the correlation between intermediary metabolism, gene expression, and oxidative stress-related proteins in long-term thermally stressed and whether they are affected by thermal stress magnitude and duration. We accordingly evaluated the gene expression profiles, in the posterior adductor muscle (PAM) and the mantle, concerning heat shock protein 70 and 90 ( and ), and the antioxidant defense indicators Mn-SOD, , , , and the metallothioneins and . Moreover, we determined antioxidant enzyme activities, oxidative stress through lipid peroxidation, and activities of intermediary metabolism enzymes. The pattern of changes in relative mRNA expression levels indicate that mussels are able to sense thermal stress even when exposed to 22°C and before mussel mortality is initiated. Data indicate a close correlation between the magnitude and duration of thermal stress with lipid peroxidation levels and changes in the activity of antioxidant enzymes and the enzymes of intermediary metabolism. The gene expression and increase in the activities of antioxidant enzymes support a scenario, according to which exposure to 24°C might trigger reactive oxygen species (ROS) production, which is closely correlated with anaerobic metabolism under hypometabolic conditions. Increase and maintenance of oxidative stress in conjunction with energy balance disturbance seem to trigger mussel mortality after long-term exposure at temperatures beyond 26°C. Eventually, in the context of preparation for oxidative stress, certain hypotheses and models are suggested, integrating the several steps of cellular stress response.
长期暴露于超过 26°C 的温度会导致贻贝死亡。本研究旨在综合说明长期热应激贻贝中介体代谢、基因表达与氧化应激相关蛋白之间的相关性,以及它们是否受到热应激幅度和时间的影响。因此,我们评估了后收肌(PAM)和套膜中热休克蛋白 70 和 90(和)以及抗氧化防御指标 Mn-SOD、、、和金属硫蛋白和的基因表达谱。此外,我们还测定了抗氧化酶活性、通过脂质过氧化引起的氧化应激以及中介代谢酶的活性。相对 mRNA 表达水平变化的模式表明,贻贝即使在暴露于 22°C 时也能够感知热应激,并且在贻贝死亡之前就已经开始了。数据表明,热应激的幅度和时间与脂质过氧化水平以及抗氧化酶和中介代谢酶活性的变化密切相关。基因表达和抗氧化酶活性的增加支持了这样一种观点,即暴露于 24°C 可能会引发活性氧(ROS)的产生,这与低代谢条件下的无氧代谢密切相关。在长期暴露于 26°C 以上温度的情况下,氧化应激的增加和维持以及能量平衡的干扰似乎会导致贻贝死亡。最终,在为氧化应激做准备的背景下,提出了一些假设和模型,整合了细胞应激反应的几个步骤。