Time-dependent effects of waterborne copper exposure influencing hepatic lipid deposition and metabolism in javelin goby Synechogobius hasta and their mechanism
Time-dependent effects of waterborne copper exposure influencing hepatic lipid deposition and metabolism in javelin goby Synechogobius hasta and their mechanism
复制标题
水性铜暴露对标枪虾虎鱼肝脏脂质沉积和代谢的时间依赖性影响及其机制
DOI：
10.1016/j.aquatox.2014.07.013
复制
发表时间：
2014-10-01
影响因子：
4.5
通讯作者：
Wu, Kun
中科院分区：
文献类型：
--
作者：
Huang, Chao;Chen, Qi-Liang;Wu, Kun
本研究旨在确定水性慢性铜（Cu）暴露对标枪虾虎鱼（Synechogobius hasta）肝脏脂质沉积和代谢的影响及其机制。 S. hasta 暴露于四种水性铜浓度（2（对照）、18、38 和 55 μg Cu/l）60 天。采样分别在第 30 天和第 60 天进行。随着铜水平的增加，存活率降低，肝脏铜含量增加。第30天，铜暴露增加了肝脏脂质含量、内脏体指数（VSI）和肝体指数（HSI）、脂肪生成酶（6PGD、G6PD、ME、ICDH和FAS）的活性以及肝脏中6PGD、G6PD、ME、FAS、ACC α、LPL、PPAR γ和SREBP-1的mRNA水平。然而，接触铜后，ATGL、HSL 和 PPAR α 的 mRNA 水平下降。第60天，Cu暴露降低了肝脂质含量、HSI、VS'、G6PD、ME、ICDH和FAS的活性以及6PGD、G6PD、ME、FAS和SREBP-1的mRNA表达，但增加了CPT 1、HSL和PPARα的mRNA表达。分别在第30天和第60天观察编码转录因子（PPARα、PPARγ和SREBP-1）的基因的转录变化与参与脂肪生成和脂肪分解的酶的活性和mRNA表达之间的差异Pearson相关性。铜暴露 30 天通过刺激脂肪生成和抑制脂肪分解诱导肝脏脂质积累。然而，60 天的铜暴露通过抑制脂肪生成和刺激脂肪分解来降低肝脏脂质含量。据我们所知，本研究首次提供了实验证据，表明水源性慢性铜暴露对鱼类中参与脂肪生成和脂肪分解代谢途径的基因以及以持续时间依赖性方式编码的酶产生了不同的影响，并为金属毒性与脂质代谢之间的关系提供了新的见解。 (C) 2014 Elsevier B.V. 保留所有权利。
The present study was conducted to determine the time-course of waterborne chronic copper (Cu) exposure effects influencing hepatic lipid deposition and metabolism in javelin goby Synechogobius hasta and their mechanisms. S. hasta were exposed to four waterborne Cu concentrations (2 (control), 18, 38 and 55 mu g Cu/l) for 60 days. Sampling occurred on day 30 and day 60, respectively. Survival decreased and hepatic Cu content increased with increasing Cu levels. On day 30, Cu exposure increased hepatic lipid content, viscerosomatic index (VSI) and hepatosomatic index (HSI), and activities of lipogenic enzymes (6PGD, G6PD, ME, ICDH and FAS) as well as the mRNA levels of 6PGD, G6PD, ME, FAS, ACC alpha, LPL, PPAR gamma and SREBP-1 in the liver. However, the mRNA levels of ATGL, HSL and PPAR alpha declined following Cu exposure. On day 60, Cu exposure reduced hepatic lipid content, HSI, VS', activities of G6PD, ME, ICDH and FAS, and the mRNA expression of 6PGD, G6PD, ME, FAS and SREBP-1, but increased mRNA expression of CPT 1, HSL and PPAR alpha. The differential Pearson correlation between transcriptional changes of genes encoding transcription factors (PPAR alpha, PPAR gamma and SREBP-1), and the activities and mRNA expression of enzymes involved in lipogenesis and lipolysis were observed on day 30 and day 60, respectively. Cu exposure for 30 days induced hepatic lipid accumulation by stimulating lipogenesis and inhibiting lipolysis. However, 60-day Cu exposure reduced hepatic lipid content by inhibiting lipogenesis and stimulating lipolysis. To our knowledge, for the first time, the present study provided experimental evidence that waterborne chronic Cu exposure differentially influenced genes involved in lipogenic and lipolytic metabolic pathway and the enzymes encoded in a duration-dependent manner in fish, and provided new insight into the relationship between metal toxicity and lipid metabolism. (C) 2014 Elsevier B.V. All rights reserved.