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左炔诺孕酮对稀有鮈鲫脂质代谢的干扰效应
引用本文:华江环,史奇朋,郭威,郭勇勇,周炳升.左炔诺孕酮对稀有鮈鲫脂质代谢的干扰效应[J].中国环境科学,2020,40(3):1345-1355.
作者姓名:华江环  史奇朋  郭威  郭勇勇  周炳升
作者单位:1. 湖北中医药大学基础医学院, 湖北 武汉 430065; 2. 中国科学院水生生物研究所, 淡水生态与生物技术国家重点实验室, 湖北 武汉 430072; 3. 中国科学院大学, 北京 100049
基金项目:湖北省自然科学基金资助项目(2018CFB324);湖北省教育厅科学技术研究项目(Q20182010);湖北中医药大学“青苗计划”项目(2017ZZX009)
摘    要:为探究孕激素左炔诺孕酮(LNG)对鱼类脂质代谢的影响,将刚孵化的稀有鮈鲫仔鱼置于0.8和6.5ng/L LNG暴露6个月至性成熟,考察其生长指标、肝脏组织病理学变化、脂质和脂蛋白含量及脂质代谢相关基因的表达情况.结果显示:(1)0.8,6.5ng/L LNG暴露显著降低70dph稀有鮈鲫的体重和肥满度,且6.5ng/L LNG暴露显著降低180dph雌、雄鱼的体长或体重;(2)0.8,6.5ng/L LNG暴露导致180dph成鱼肝脏出现细胞空泡、肝细胞肿胀等损伤;(3)0.8,6.5ng/L LNG暴露显著降低180dph雌鱼肝脏中甘油三酯、胆固醇的含量,且6.5ng/L LNG暴露显著降低雌鱼血浆中甘油三酯的含量,但对雄鱼肝脏及血浆的脂质含量无显著影响;(4)0.8,6.5ng/L LNG暴露显著降低180dph雌鱼肝脏中脂肪酸合成酶基因(fasn) mRNA的表达水平,且6.5ng/L LNG暴露显著降低180dph雄鱼肝脏中fasn及乙酰辅酶A羧化酶基因(acaca) mRNA的表达水平.由此可见,LNG长期低剂量暴露可抑制稀有鮈鲫的生长、诱导肝细胞损伤、引起肝脏和血浆脂质含量发生性别差异性变化,并影响肝脏中脂质代谢相关基因的表达,表明LNG在低浓度下可干扰稀有鮈鲫的脂质代谢,提示LNG对鱼类种群具有较高的潜在生态风险.

关 键 词:孕激素  左炔诺孕酮  脂质代谢  稀有鮈鲫  长期暴露  
收稿时间:2019-08-15

Disrupting effects of levonorgestrel on lipid metabolism in Chinese rare minnow
HUA Jiang-huan,SHI Qi-peng,GUO Wei,GUO Yong-yong,ZHOU Bing-sheng.Disrupting effects of levonorgestrel on lipid metabolism in Chinese rare minnow[J].China Environmental Science,2020,40(3):1345-1355.
Authors:HUA Jiang-huan  SHI Qi-peng  GUO Wei  GUO Yong-yong  ZHOU Bing-sheng
Institution:1. School of Basic Medical Sciences, Hubei University of Chinese Medicine, Wuhan 430065, China; 2. State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China; 3. University of Chinese Academy of Sciences, Beijing 100049, China
Abstract:In order to explore the effects of progestin levonorgestrel (LNG) on lipid metabolism in fish, newly hatched Chinese rare minnow larvae were exposed to 0.8 and 6.5ng/L LNG for 6months until adults, and the growth parameters, hepatic histopathologic changes, lipids and lipoproteins contents and expression levels of lipid metabolism related genes were investigated. The results showed that the body weights and condition factors of rare minnow at 70dph were significantly decreased by exposure to 0.8 and 6.5ng/L LNG, and the body lengths or body weights were also significantly decreased in females and males at 180dph after exposure to 6.5ng/L LNG. Hepatic damages such as cellular vacuolation and swelling of hepatocytes were induced in adults at 180dph after exposure to 0.8 and 6.5ng/L LNG. The hepatic triglyceride and cholesterol contents in females at 180dph were significantly decreased by exposure to 0.8 and 6.5ng/L LNG, and the serum triglyceride contents were also significantly decreased after exposure to 6.5ng/L LNG, but no effects were observed on male hepatic and serum lipid contents. Besides, the hepatic mRNA expression level of fatty acid synthase gene (fasn) was significantly decreased in females at 180dph by exposure to 0.8 and 6.5ng/L LNG, and the hepatic mRNA expression levels of fasn and acetyl-CoA carboxylase gene (acaca) were also significantly decreased in males at 180dph after exposure to 6.5ng/L LNG. As can be concluded from the results, long-term exposure of rare minnow to low concentrations of LNG inhibited growth, induced hepatic damages, caused sex-specific changes on hepatic and serum lipid contents, and affected mRNA expression of lipid metabolism related genes in the liver. The present study demonstrates that LNG could disrupt lipid metabolism in rare minnow at low concentrations, indicating high potential ecological risks of LNG to fish populations.
Keywords:progestin  levonorgestrel  lipid metabolism  Chinese rare minnow  long-term exposure  
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