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溶解氧对线纹海马幼鱼氨氮耐受性的影响及氨氮胁迫下鳃、肝脏组织结构的变化

罗辉玉1,吴水清1,郑乐云1*,林金波2,王全阳3   

  1. 1福建省水产研究所, 福建省海洋生物增养殖与高值化利用重点实验室, 福建厦门 361013;2厦门小嶝水产科技有限公司, 福建厦门 361104;3东山县海洋与渔业局, 福建漳州 363400)
  • 出版日期:2020-03-10 发布日期:2020-03-10

Effects of dissolved oxygen on tolerance of juvenile Hippocampus erectus to ammonia-N and histopathology of gill and liver under ammonia-N stress.

LUO Hui-yu1, WU Shui-qing1, ZHENG Le-yun1*, LIN Jin-bo2, WANG Quan-yang3   

  1. (1Key Laboratory of Cultivation and Highvalue Utilization of Marine Organisms in Fujian Province, Fisheries Research Institute of Fujian, Xiamen 361013, Fujian, China; 2Xiamen Xiaodeng Aquatic Science and Technology, Co., Ltd. Xiamen 361104, Fujian, China; 3Ocean and Fisheries Administration of Dongshan County, Zhangzhou 363400, Fujian, China).
  • Online:2020-03-10 Published:2020-03-10

摘要: 为了解氨氮对线纹海马(Hippocampus erectus)幼鱼的毒理影响,本实验探讨了在正常溶解氧(4.32~5.12 mg·L-1)和高溶解氧(8.22~9.46 mg·L-1)条件下,线纹海马幼鱼的氨氮半致死浓度,以及6、9、12 mg·L-1的氨氮溶液胁迫下线纹海马幼鱼的鳃、肝脏组织结构的变化。结果表明:正常溶解氧条件下,氨氮对线纹海马幼鱼96 h半致死浓度(96 h LC50)为10.22 mg·L-1,安全浓度(SC)为1.02 mg·L-1;非离子氨的半致死浓度(96 h LC50)为0.16 mg·L-1,安全浓度(SC)为0.016 mg·L-1;高溶解氧条件下,氨氮对幼鱼的96 h LC50为12.68 mg·L-1,SC为1.27 mg·L-1;非离子氨96 h LC50为0.2 mg·L-1,SC为0.02mg·L-1。氨氮胁迫造成线纹海马幼鱼鳃组织在不同时间出现鳃丝血管扩张、泌氯细胞增生,鳃小片基部毛细血管破裂、红细胞溢出、鳃组织充血变性、卷曲变短、呼吸上皮细胞变性脱落等现象,并使肝脏肝细胞出现肿胀、细胞核肿大,肝血窦扩张、细胞轮廓模糊等组织变化;随着胁迫物浓度和胁迫时间增加,肝组织出现水样变性、空泡化、溶解,导致肝组织变得松散无序。综上,适当提高溶解氧能有效减轻氨氮对线纹海马幼鱼的毒性,超过阈值的氨氮胁迫会损害线纹海马幼鱼的鳃和肝脏组织结构。

关键词: 产量, 土传病害, 嫁接, 根际土壤环境, 辣椒

Abstract: We investigated the toxic effects of ammonia-N on juvenile lined seahorse (Hippocampus erectus). The half lethal concentration of ammonia-N to lined seahorses for 96 hours (96 h LC50) was evaluated under normal oxygen level (4.32-5.12 mg·L-1) and high oxygen level (8.22-9.46 mg·L-1), respectively. We examined the histopathological changes of gill and liver of juvenile lined seahorses under ammonia-N stress (control, 6, 9, 12 mg·L-1). The results showed that the 96h LC50 of ammonia-N and non-ionic ammonia to juvenile lined seahorses at normal oxygen level was 10.22 and 0.16 mg·L-1, with a safe concentration of 1.02 and 0.016 mg·L-1, respectively. When treated with high dissolved oxygen, the 96h LC50 of ammonia-N and nonionic ammonia to juvenile lined seahorses increased to 12.68 and 0.2 mg·L-1, with a safety upper limit of 1.27 and 0.02 mg·L-1, respectively. The juvenile lined seahorses exposed to ammonia displayed histopathologic abnormalities in gill and liver, which were dependent on dose and duration. AmmoniaN stress caused gill lesions, including telangiectasis, vascular congestion and fracture, necrosis of epithelial cell and hyperplasia of chloride cells. Nucleomegaly, hepatocytes swelling, sinusoids dilatation and blurred cell contour were observed in liver. The enhancement of ammonia-N stress increased liver lesions, causing hydropic degeneration, dissolution and vacuolation of hepatocytes, resulting in loose organization of hepatic tissue. In summary, ammonia nitrogen stress above threshold to juvenile lined seahorse would damage the structure of gill and liver tissue. Appropriately increasing the concentration of dissolved oxygen could effectively alleviate the toxicity of ammonia N on juvenile lined seahorse.

Key words: yield., pepper, rhizosphere soil environment, grafting, root-borne disease