| 王贞杰,陈四清,曹栋正,卢 斌,常 青,刘长琳,燕敬平.急性氨氮胁迫对圆斑星鲽(Verasper variegatus)幼鱼鳃和肝组织结构及相关酶活性的影响.渔业科学进展,2017,38(2):59-69 |
| 急性氨氮胁迫对圆斑星鲽(Verasper variegatus)幼鱼鳃和肝组织结构及相关酶活性的影响 |
| Effects of Acute Ammonia Nitrogen Stress on Histopathology of Gill and Liver and Enzyme Activities of Juvenile Verasper variegatus |
| 投稿时间：2015-12-01 修订日期：2016-01-10 |
| DOI：10.11758/yykxjz.20151201001 |
| 中文关键词: 圆斑星鲽 氨氮胁迫 组织结构 酶活性 |
| 英文关键词: Verasper variegatus Ammonia nitrogen stress Organizational structure Enzyme activity |
| 基金项目:山东省自主创新成果转化专项(2013ZHZX2A0803)资助 |
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| 中文摘要: |
| 本实验以体重为(70.0±5.5) g圆斑星鲽(Verasper variegatus)幼鱼为研究对象，研究了不同浓度氨氮胁迫对其鳃、肝组织及相关酶活性的影响。实验首先进行96 h急性氨氮胁迫，得出96 h LC50，在此基础上，设置对照和低(35 mg/L)、中(50 mg/L)、高(65 mg/L) 3个氨氮浓度处理组，进行6、12、24、48和96 h的氨氮胁迫。结果显示，氨氮胁迫下，鳃小片基部泌氯细胞、呼吸上皮细胞水肿变性、坏死和脱落，鳃腔充血，柱状细胞排列不整齐；毛细血管破裂，红细胞溢出；鳃小片变粗、变短并卷曲。肝细胞核出现偏移、肿大和溶解现象，细胞轮廓模糊，血窦扩张、充血形成点状病灶，细胞水样变性、空泡化。Na+/K+-ATP酶、谷胱甘肽过氧化物酶(GSH-PX)活力均与对照组差异显著(P<0.05)；超氧化物歧化酶(SOD)活力显著高于对照组(P<0.05)；氨氮胁迫组96 h丙二醛(MDA)浓度均高于对照组，且与氨氮浓度呈显著正相关(P<0.05)；氨氮胁迫对血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、溶菌酶(LSZ)产生显著性影响(P<0.05)。肝脏ALT、AST、LSZ活性96 h均显著低于对照组(P<0.05)。研究表明，氨氮胁迫对圆斑星鲽产生损害，氨氮胁迫使鱼体抗氧化系统、非特异性免疫系统下降，正常生理代谢受到阻碍，鳃组织损伤，呼吸功能受损。肝组织充血形成点状病灶，机体新陈代谢和解毒功能下降。 |
| 英文摘要: |
| Ammonia is a major source of water pollution and a cause of fish diseases. The object of this study was to evaluate the effects of ammonia-N stress on the gill Na+/K+-ATPase, the liver microstructure, and serum physiological-biochemical indices of juvenile Verasper variegatus. Experimental fish had an initial average weight of (70.0±5.5) g. Subjects were first exposed to ammonia-N for 96 hours to obtain the median lethal concentration at 96 h. According to the data, we set up a control group and three ammonia-N treatments of which the concentrations were 35 mg/L (low group), 50 mg/L (middle group), and 65 mg/L (high group). In each group the subjects were treated for a series of periods (0, 6, 12, 24, 48 and 96 h). In the gill microstructure, the ammonia-N stress caused changes such as the increase in chloride cells, the shedding of pavement cells, epithelial tissue hyperplasia, the fracture in blood capillaries, the overflow of red blood cells, shortening and curling of thickened gill dice, and the breakage and congestion of the gill cavity. In liver tissue, we observed dissolution of liver nuclei, vacuoles in cells, liver cell degeneration, liquidized cells, blood sinus expansion, hyperemia, and severe congestion. Under the ammonia-N stress the activities of Na+/K+-ATPase and glutathione peroxidase (GSH-PX) were first decreased and then increased, which was significantly different from the control group (P<0.05). The superoxide dismutase (SOD) activity was raised followed by a decrease, and was higher than the control group (P<0.05). After 96-hour treatment with ammonia nitrogen, the malondialdehyde (MDA) concentration became higher than the control group, and there was a positive correlation between the MDA concentration and ammonia nitrogen concentration (P<0.05). Ammonia nitrogen stress also resulted in an increase-decrease change in activities of serum alanine amino transferase (ALP), aspartate amino transferase (AST) and lysozyme (LSZ) (P<0.05). After 96-hour treatment, activities of liver ALT and AST first increased and then decreased, and was significantly lower than the control group (P<0.05). The liver LSZ activity was significantly lower than the control group after 96-hour treatment (P<0.05). These results suggested that ammonia nitrogen stress could cause a variety of impairments in the fish body, including deterioration of the antioxidant system, nonspecific immune system, physiological metabolism, the gill tissue, the respiratory function and the detoxification function. Also it led to the liver tissue hyperemia and the formation of dot lesions. |
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