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氟暴露下泽蛙幼体肝脏的形态变化和分子生物标志物反应。

The morphological changes and molecular biomarker responses in the liver of fluoride-exposed Bufo gargarizans larvae.

机构信息

College of Life Science, Shaanxi Normal University, Xi'an 710119, China.

College of Life Science, Shaanxi Normal University, Xi'an 710119, China.

出版信息

Ecotoxicol Environ Saf. 2018 Apr 30;151:199-205. doi: 10.1016/j.ecoenv.2018.01.027. Epub 2018 Feb 4.

DOI:10.1016/j.ecoenv.2018.01.027
PMID:29367176
Abstract

The goal of the current study was to evaluate the negative influences of fluoride on liver of Bufo gargarizans larvae. B. gargarizans larvae were treated with 42.4mgF/L for 0, 24, 48 and 72h at Gosner stage 37. The morphological changes and responses of molecular biomarkers involved in lipid metabolism, oxidative stress and apoptosis were examined in liver. Disappearance of cell boundaries, degeneration of hepatic parenchyma cells and significant increase in the number of melanomacrophage centres and the quantity of lipid droplets were found in the liver treated with 42.4mgF/L for 72h. In addition, in the relative expression of acetyl CoA carboxylase 1 (ACC-1), fatty acid elongase 1 (FAE-1), sterol carrier protein 2 (SCP-2), and carnitine palmitoyltransferase-1 (CPT-1), decrease was observed after 24, 48 and 72h of 42.4mgF/L exposure. Furthermore, the transcript levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were downregulated in tadpoles exposed for 24, 48 and 72h to 42.4mgF/L, while the transcript level of heat shock protein 90 (HSP90) was upregulated at 42.4mgF/L for 72h. Also, mRNA expression of Bcl-2-associated transcription factor 1(BCLAF1) and thyroid hormone receptors (TRα and TRβ) was significantly upregulated in tadpoles treated with 42.4mgF/L for 72h. Therefore, our results suggested that the liver injury induced by fluoride might result from disruption of lipid metabolism, oxidative damage and apoptosis.

摘要

本研究旨在评估氟化物对中华大蟾蜍(Bufo gargarizans)幼体肝脏的负面影响。将中华大蟾蜍幼体暴露于 42.4mgF/L 氟化物中,分别在 0、24、48 和 72h 时处于 Gosner 发育阶段 37 期。在肝脏中检测了参与脂质代谢、氧化应激和细胞凋亡的分子生物标志物的形态变化和反应。结果发现,与对照组相比,在暴露于 42.4mgF/L 氟化物 72h 的肝脏中,细胞边界消失,肝实质细胞变性,黑色素巨噬细胞中心数量显著增加,脂滴数量增多。此外,在乙酰辅酶 A 羧化酶 1(ACC-1)、脂肪酸延长酶 1(FAE-1)、固醇载体蛋白 2(SCP-2)和肉碱棕榈酰转移酶 1(CPT-1)的相对表达中,在暴露于 42.4mgF/L 24、48 和 72h 后观察到下降。此外,在暴露于 42.4mgF/L 24、48 和 72h 的幼体中,超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPx)的转录水平下调,而热休克蛋白 90(HSP90)的转录水平在 42.4mgF/L 暴露 72h 时上调。此外,在暴露于 42.4mgF/L 72h 的幼体中,Bcl-2 相关转录因子 1(BCLAF1)和甲状腺激素受体(TRα 和 TRβ)的 mRNA 表达显著上调。因此,我们的研究结果表明,氟化物引起的肝脏损伤可能是由于脂质代谢紊乱、氧化损伤和细胞凋亡所致。

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