Xu Dan, Tang Yongzheng, Li Wenlong, Yang Yingming
School of Ocean, Yantai University, Yantai 264005, China.
Key Laboratory for Sustainable Development of Marine Fisheries, Ministry of Agriculture and Rural Affairs, Yellow Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, 106 Nanjing Road, Qingdao 266071, China.
Animals (Basel). 2023 Dec 6;13(24):3768. doi: 10.3390/ani13243768.
As the largest green macroalgal bloom in the Yellow Sea of China, the overgrowth and degradation of (. ) have a harmful effect on marine organisms and the aquaculture industry. However, the regulation mechanism of stress on the antioxidant capacity and inflammatory response of marine fish is still not completely understood. A 15-day exposure experiment was conducted to evaluate the effects of stress on the antioxidant capacity and inflammatory response of the Japanese flounder () (283.11 ± 6.45 g). The results showed that . stress significantly decreased their survival rate. Serum total antioxidant capacity (T-AOC) and non-specific immune-related enzyme activities were significantly impacted under . conditions. Moreover, . stress significantly decreased T-AOC, superoxide dismutase (SOD) activity, and catalase (CAT) activities in the liver, while malondialdehyde (MDA) contents were significantly increased. Similarly, antioxidant-related gene (, and ) expressions were synchronously downregulated in the liver under . stress. Furthermore, . stress significantly upregulated pro-inflammatory gene (, , , and ) expressions and the phosphorylation levels of the p38 and JNK MAPK pathways in the head kidney. In addition, endoplasmic reticulum (ER) stress-related gene and protein expressions were also upregulated in the head kidney. Overall, these results revealed that stress suppressed the antioxidant capacity and induced an inflammatory response in the Japanese flounder. This study could advance the understanding of the adverse effects of . stress on marine benthic fish and promote the sustainable development of aquaculture.
作为中国黄海最大规模的大型绿藻爆发,(此处原文括号内容缺失,无法准确翻译)的过度生长和降解对海洋生物和水产养殖业产生了有害影响。然而,(此处原文括号内容缺失,无法准确翻译)胁迫对海洋鱼类抗氧化能力和炎症反应的调控机制仍未完全明确。进行了一项为期15天的暴露实验,以评估(此处原文括号内容缺失,无法准确翻译)胁迫对牙鲆(283.11 ± 6.45克)抗氧化能力和炎症反应的影响。结果表明,(此处原文缺失具体结果内容,无法准确翻译)胁迫显著降低了它们的存活率。在(此处原文括号内容缺失,无法准确翻译)条件下,血清总抗氧化能力(T-AOC)和非特异性免疫相关酶活性受到显著影响。此外,(此处原文括号内容缺失,无法准确翻译)胁迫显著降低了肝脏中的T-AOC、超氧化物歧化酶(SOD)活性和过氧化氢酶(CAT)活性,而丙二醛(MDA)含量显著增加。同样,在(此处原文括号内容缺失,无法准确翻译)胁迫下,肝脏中抗氧化相关基因(此处原文括号内容缺失,无法准确翻译)的表达同步下调。此外,(此处原文括号内容缺失,无法准确翻译)胁迫显著上调了头肾中促炎基因(此处原文括号内容缺失,无法准确翻译)的表达以及p38和JNK丝裂原活化蛋白激酶(MAPK)途径的磷酸化水平。此外,头肾中内质网(ER)应激相关基因和蛋白表达也上调。总体而言,这些结果表明(此处原文括号内容缺失,无法准确翻译)胁迫抑制了牙鲆的抗氧化能力并诱导了炎症反应。本研究有助于增进对(此处原文括号内容缺失,无法准确翻译)胁迫对海洋底栖鱼类不利影响的理解,并促进水产养殖业的可持续发展。