Key Laboratory of Freshwater Animal Breeding, Ministry of Agriculture of P.R.C., Fishery College, Huazhong Agricultural University, Wuhan 430070, China.
Aquat Toxicol. 2013 May 15;132-133:173-81. doi: 10.1016/j.aquatox.2013.02.002. Epub 2013 Mar 1.
The present study is conducted to determine the potential mechanisms of Zn on hepatic lipid deposition and metabolism for yellow catfish Pelteobagrus fulvidraco with 8-week chronic exposure to low Zn levels (Zn levels: 0.05, 0.35 and 0.86mg/l Zn, respectively) and 96-h acute exposure to a high Zn level (Zn level: 4.71mg/l Zn, respectively). For that purpose, hepatic lipid deposition and Zn accumulation, hepatic carnitine palmitoyltransferase I (CPT I) and lipoprotein lipase (LPL) activities, and the hepatic mRNA expression of ten genes involved in lipid metabolism are determined. Chronic (8 weeks) exposure to low Zn levels apparently increases hepatic lipid content, hepatosomatic index (HSI) (P<0.05) and LPL activity, and reduces hepatic CPT I activity. In contrast, the acute (96h) exposure to high Zn level reduces hepatic lipid content, HSI and LPL activity, and increases CPT I activity. The change of mRNA levels of genes related to lipid metabolism is Zn concentration-dependent. Pearson correlations among mRNA expression levels, lipid content, CPT I and LPL activities in liver are also observed in yellow catfish with the 8-week chronic Zn exposure. For the first time, our study demonstrates the effect of waterborne Zn exposure on lipid metabolism at the molecular levels in fish, which may contribute to understanding the mechanism of Zn-induced hepatic toxicity in fish.
本研究旨在确定锌对黄颡鱼肝脏脂质沉积和代谢的潜在机制，采用 8 周慢性低锌水平（锌水平分别为 0.05、0.35 和 0.86mg/L）和 96 小时急性高锌水平（锌水平分别为 4.71mg/L）暴露的方法进行。为此，测定了肝脏脂质沉积和锌积累、肝脏肉碱棕榈酰转移酶 I（CPT I）和脂蛋白脂肪酶（LPL）活性以及参与脂质代谢的十个基因的肝脏 mRNA 表达。慢性（8 周）暴露于低锌水平明显增加了肝脏脂质含量、肝体比（HSI）（P<0.05）和 LPL 活性，降低了肝脏 CPT I 活性。相比之下，急性（96h）暴露于高锌水平降低了肝脏脂质含量、HSI 和 LPL 活性，增加了 CPT I 活性。与脂质代谢相关的基因的 mRNA 水平的变化与锌浓度有关。在黄颡鱼的 8 周慢性锌暴露中，还观察到了 mRNA 表达水平、肝脏脂质含量、CPT I 和 LPL 活性之间的皮尔逊相关性。本研究首次证明了水相锌暴露对鱼类脂质代谢的分子水平的影响，这可能有助于理解锌诱导鱼类肝毒性的机制。
