Effect of waterborne copper exposure on growth, hepatic enzymatic activities and histology in Synechogobius hasta.
Effect of waterborne copper exposure on growth, hepatic enzymatic activities and histology in Synechogobius hasta.
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DOI：
10.1016/j.ecoenv.2010.06.019
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发表时间：
2010-09
影响因子：
6.8
通讯作者：
X. Liu;Z. Luo;B.-X. Xiong;X. Liu;Y. Zhao;G. Hu;G. Lv
中科院分区：
文献类型：
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作者：
X. Liu;Z. Luo;B.-X. Xiong;X. Liu;Y. Zhao;G. Hu;G. Lv
本研究通过测定海水铜浓度分别为0（对照）、0.15和0.3mgCu/L，暴露15 d后，尖吻集虎鱼的生长、肝酶活性和组织学变化，探讨海水铜暴露是否会诱发该鱼类脂肪肝综合征。生长（WG和SGR）下降，但HSI增加在S。Hasta随水体铜水平的升高而升高（P<0.05）。水体铜暴露还显著增加了全身和肝脏中的脂质含量，降低了蛋白质含量，并增加了全身和脊椎中铜的积累。结果表明，铜暴露改变了肝酶（SOD、CAT、SDH、PK、LDH、LPL和HL）的活性，增加了肝脂质过氧化水平，破坏了鳃和肝的组织结构。再见因此，我们的研究首次表明，水载铜暴露可诱导鱼类脂肪肝综合征。
The present study was conducted to determine growth, hepatic enzymatic activities and histology in Synechogobius hasta exposed to waterborne copper concentrations of 0 (control), 0.15 and 0.3mgCu/l, respectively, for 15 days, and explore whether waterborne copper exposure could induce the fatty liver syndrome for the fish species. Growth (WG and SGR) declined, but HSI increased in S. hasta with increasing waterborne copper levels (P<0.05). Waterborne copper exposure also significantly increased lipid content and reduced protein content in both whole body and liver, and increased copper accumulation in whole body and vertebrae. Copper exposure changed hepatic enzymatic activities (SOD, CAT, SDH, PK, LDH, LPL and HL) and increased hepatic lipid peroxidation level, impaired the histological structure of the gill and liver in S. hasta. Thus, our study demonstrated for the first time that waterborne Cu exposure could induce fatty liver syndrome in fish.