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首页> 外文期刊>Aquaculture Research >Effects of ammonia stress on liver microstructure, antioxidant capability and inflammation‐related genes and post‐exposure recovery in the hybrid sturgeon (Acipenser baerii ♀ × Acipenser schrencki ♂)
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Effects of ammonia stress on liver microstructure, antioxidant capability and inflammation‐related genes and post‐exposure recovery in the hybrid sturgeon (Acipenser baerii ♀ × Acipenser schrencki ♂)

机译:氨胁迫对杂交鲟(Acipenser baerii ♀ × Acipenser schrencki ♂)肝脏微观结构、抗氧化能力、炎症相关基因及暴露后恢复的影响

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Abstract Ammonia is an important water quality factor, which causes several adverse effects in fish. In this study, the 5‐month‐old hybrid sturgeon (Acipenser baerii ♀ × Acipenser schrencki ♂) with a mean body weight of 50 ± 0.5 g was subjected to ammonia stress (0 mg/L, control group; 10 mg/L, low‐concentration group; 50 mg/L, high‐concentration group) for 48 h and followed by recovery for 48 h, changes of liver tissue, antioxidant enzyme activity and relative expressions of inflammation‐related genes were observed. The results showed that, with an increasing ammonia concentration and exposure duration, hepatocytes showed swelling, congestion and indistinguishable cellular outline. After 48 h of recovery, the degree of swelling decreased, nuclear shifted, and vacuolation reduced; however, the normal levels before stress application were not reached again. Additionally, compared with the control group, the activities of superoxide dismutase, catalase and glutathione peroxidase were significantly upregulated 6 h after stress. Malondialdehyde reached the maximum at 24 h in the low‐concentration group and at 12 h in the high‐concentration group, indicating the activity of the antioxidant system trying to protect cells from oxidative stress. Furthermore, the relative expression levels of interleukin 1 beta, tumour necrosis factor α genes and heat shock proteins (both HSP70 and HSP90β) in the liver were induced by ammonia stress. These results provide direct evidence for the damage caused by ammonia stress and the self‐recovery ability of the hybrid sturgeon.
机译:摘要 氨是重要的水质因子,对鱼类造成多种不良影响。本研究以平均体重为50±0.5 g的5月龄杂交鲟鱼(Acipenser baerii ♀ × Acipenser schrencki ♂)为例,在氨胁迫下(0 mg/L,对照组;10 mg/L,低浓度组;50 mg/L,高浓度组)48 h,随后恢复48 h, 观察肝组织、抗氧化酶活性和炎症相关基因的相对表达变化。结果表明,随着氨浓度的增加和暴露时间的增加,肝细胞出现肿胀、充血和难以区分的细胞轮廓。恢复48 h后,肿胀程度降低,核移位,空泡减少;然而,没有再次达到施加压力前的正常水平。与对照组相比,胁迫后6 h超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶活性显著上调。丙二醛在低浓度组24 h和高浓度组12 h时达到最大值,表明抗氧化系统试图保护细胞免受氧化应激的活性。此外,氨胁迫诱导肝脏中白细胞介素1β、肿瘤坏死因子α基因和热休克蛋白(HSP70和HSP90β)的相对表达水平。这些结果为杂交鲟的氨胁迫造成的损害和自我恢复能力提供了直接证据。

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