Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, 7 Nanhai Road, Qingdao, 266071, China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, Qingdao, 266237, China; University of Chinese Academy of Sciences, 19 Yuquan Road, Beijing, 100049, China.
Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, 7 Nanhai Road, Qingdao, 266071, China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, Qingdao, 266237, China.
Fish Shellfish Immunol. 2018 May;76:27-34. doi: 10.1016/j.fsi.2018.02.001. Epub 2018 Feb 11.
White shrimp Litopenaeus vannamei were reared under conditions of gradual changes to a low pH (gradual-low pH, 6.65-8.20) or a high pH (gradual-high pH, 8.20-9.81) versus a normal pH environment (8.14-8.31) during a 28-day period. Survival of shrimp, and ROS production, antioxidant responses and oxidative damage in the hepatopancreas and midgut were investigated. Consequently, shrimp enhanced MnSOD, GPx, and Hsp70 transcripts as early defense mechanism in the hepatopancreas and midgut to scavenge excessive ROS during short-term (≤ 7 days) gradual-low and high pH stress. Meanwhile, the hepatopancreas was more sensitive to ROS than midgut because of earlier ROS production increase, antioxidant response and oxidative damage. Then, suppressed antioxidant response in the hepatopancreas and midgut of shrimp suggested a loss of antioxidant regulatory capacity caused by aggravated oxidative damage after long-term (≥ 14 days) gradual-high pH stress, leading to continuous death. However, enhanced GPx, GST, and Hsp70 transcripts in the hepatopancreas and midgut might be long-term(≥ 14 days) antioxidant adaptation mechanism of shrimp to gradual-low pH stress, which could prevent further ROS perturbation and weaken oxidative damage to achieve a new immune homeostasis, contributing to stable survival rate. Therefore, we have a few insights that it is necessary to protect hepatopancreas for controlling shrimp death under gradual-high pH stress.
凡纳滨对虾在 28 天的时间内,分别在低 pH(逐渐低 pH,6.65-8.20)或高 pH(逐渐高 pH,8.20-9.81)条件下逐渐适应低 pH 或高 pH 环境(8.14-8.31)。研究了虾的存活率、ROS 产生、抗氧化反应和肝胰腺及中肠的氧化损伤。结果表明,虾在短期(≤7 天)逐渐低 pH 和高 pH 应激时,通过 MnSOD、GPx 和 Hsp70 转录本增强早期防御机制,在肝胰腺和中肠中清除过多的 ROS。同时,由于 ROS 产生较早增加、抗氧化反应和氧化损伤,肝胰腺比中肠对 ROS 更为敏感。然后,长期(≥14 天)逐渐高 pH 应激导致虾肝胰腺和中肠抗氧化反应受到抑制,表明抗氧化调节能力丧失,氧化损伤加剧,导致持续死亡。然而,肝胰腺和中肠中 GPx、GST 和 Hsp70 转录本的增强可能是虾对逐渐低 pH 应激的长期(≥14 天)抗氧化适应机制,可防止 ROS 进一步扰动,减轻氧化损伤,达到新的免疫稳态,有助于稳定的存活率。因此,我们有一些见解,即在逐渐高 pH 应激下,保护肝胰腺对于控制虾的死亡是必要的。