Fishery College, Huazhong Agricultural University, Wuhan 430070, China.
Ecotoxicol Environ Saf. 2011 Oct;74(7):1864-73. doi: 10.1016/j.ecoenv.2011.06.018. Epub 2011 Jul 20.
The present study was conducted to determine the metal accumulation, antioxidant enzymatic response, hepatic intermediary metabolism and histological changes in Synechogobius hasta exposed to 0.35 (control), 9.7 and 19.2mg/L Zn, respectively, on the 0, 4th, 8th and 12th day. Waterborne Zn exposure significantly reduced hepatosomatic index, hepatic lipid contents and fatty liver occurrence rate, increased Zn, Fe and Mn contents and reduced the contents of Cu and Ca in liver, and increased muscle Zn content. Waterborne Zn exposure also significantly influenced enzymatic activities involved in antioxidant responses (superoxide dismutase, catalase, glutathione-S-transferase, malondialdehyde) in liver and spleen, and changed hepatic intermediary enzymatic activities (succinate dehydrogenase, malic dehydrogenase, lactate dehydrogenase, lipoprotein lipase, hepatic lipase), impaired the histological structure of the gill and spleen, and reduced vacuolated hepatocytes. Thus, our study demonstrated for the first time that waterborne Zn exposure could reduce fatty liver syndrome in S. hasta.
本研究旨在确定暴露于 0.35（对照）、9.7 和 19.2mg/L Zn 下的后肛鱼（Synechogobius hasta）的金属积累、抗氧化酶反应、肝中间代谢和组织学变化。在第 0、4、8 和 12 天，水基 Zn 暴露显著降低了肝体指数、肝脂含量和脂肪肝发生率，增加了 Zn、Fe 和 Mn 含量，降低了肝中 Cu 和 Ca 的含量，并增加了肌肉中的 Zn 含量。水基 Zn 暴露还显著影响了肝脏和脾脏中参与抗氧化反应的酶活性（超氧化物歧化酶、过氧化氢酶、谷胱甘肽-S-转移酶、丙二醛），改变了肝中间代谢酶活性（琥珀酸脱氢酶、苹果酸脱氢酶、乳酸脱氢酶、脂蛋白脂肪酶、肝脂肪酶），损害了鳃和脾脏的组织结构，并减少了空泡化的肝细胞。因此，我们的研究首次表明，水基 Zn 暴露可减少后肛鱼的脂肪肝综合征。
