Wang Jing, Dong Bo, Yu Zhen-Xing, Yao Cui-Luan
Fisheries College, Jimei University, Xiamen 361021, China.
College of Marine Life Science, Ocean University of China, Qingdao 266003, China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, Qingdao 266237, China.
Comp Biochem Physiol A Mol Integr Physiol. 2018 Aug;222:7-15. doi: 10.1016/j.cbpa.2018.04.001. Epub 2018 Apr 11.
Examining the physiological responses of mussels to thermal stress is crucial to evaluate their biogeographic distribution and ability to adapt to a changing climate. In the present study, we investigated the effects of acute cold (8 °C and 15 °C) and heat (35 °C and 42 °C) stress on the mortality rate, reactive oxygen species (ROS) production, malondialdehyde (MDA) content, mitochondrial membrane potential (MMP) and antioxdative responses in the gill tissue of the green mussel species Perna viridis. Our results showed that cold and heat stress induced a temperature-dependent increase in mortality rate. ROS production increased significantly (p < 0.01) after both cold and heat stress. However, the activities of antioxidant enzymes, including SOD, CAT and GSH-Px, were greatly enhanced only after heat stress. In addition, MDA content and MMP increased significantly under both cold and heat stress. The up-regulation of Hsp70 transcripts was only detected after acute stress at 35 °C. However, p38-MAPK phosphorylation levels increased after both cold and heat stress. In addition, a moderate activation of caspase-3 was found after mussels were exposed to 8 °C and 42 °C stress. Our results suggest that both extreme cold and heat stress could induce ROS production in the gill tissue of P. viridis, which might result in lipid peroxidation and mitochondria dysfunction. Antioxidative enzymes and Hsp70 might be important in the heat stress response of animals, whereas p38-MAPK might be crucial in the acute response to both cold and heat stress. However, caspase-3 activation might be very weak under both cold and heat stress.
研究贻贝对热应激的生理反应对于评估其生物地理分布和适应气候变化的能力至关重要。在本研究中，我们调查了急性冷应激（8°C和15°C）和热应激（35°C和42°C）对翡翠贻贝鳃组织中死亡率、活性氧（ROS）产生、丙二醛（MDA）含量、线粒体膜电位（MMP）和抗氧化反应的影响。我们的结果表明，冷应激和热应激均导致死亡率随温度升高而增加。冷应激和热应激后ROS产生均显著增加（p<0.01）。然而，抗氧化酶（包括超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶）的活性仅在热应激后大幅增强。此外，冷应激和热应激下MDA含量和MMP均显著增加。仅在35°C急性应激后检测到热休克蛋白70（Hsp70）转录本上调。然而，冷应激和热应激后p38丝裂原活化蛋白激酶（p38-MAPK）磷酸化水平均升高。此外，贻贝暴露于8°C和42°C应激后发现半胱天冬酶-3（caspase-3）有适度激活。我们的结果表明，极端冷应激和热应激均可诱导翡翠贻贝鳃组织中ROS产生，这可能导致脂质过氧化和线粒体功能障碍。抗氧化酶和Hsp70可能在动物热应激反应中起重要作用，而p38-MAPK可能在冷应激和热应激的急性反应中起关键作用。然而，冷应激和热应激下caspase-3激活可能非常微弱。
