School of Environmental Science and Engineering, Chang'an University, Xi'an, 710064 China; Key Laboratory of Subsurface Hydrology and Ecological Effects in Arid Region of Ministry of Education, Chang'an University, Xi'an, 710064 China.
College of Life Sciences, Shaanxi Normal University, Xi'an 710062, China.
Chemosphere. 2017 Sep;182:255-266. doi: 10.1016/j.chemosphere.2017.05.040. Epub 2017 May 7.
In the current study, the adverse effects of TCS on liver health of B. gargarizans tadpoles were assessed. B. gargarizans larvae were exposed to TCS at 0, 10, 30, 60, and 150 μg L from Gosner stage 3 until metamorphic climax. The hepatosomatic index (HSI), hepatic histological and ultrastructural features, and transcript levels of genes associated with detoxification and oxidative stress as well as lipid metabolism in the livers were determined. Exposure to 150 μg L TCS resulted in increased HSI of tadpoles at metamorphic climax. Histological changes characterized by an increase in the number of melanomacrophage, nucleus pyknosis, and deposition of collagen fibers were observed in liver at 60 and 150 μg L TCS. Moreover, marked ultrastructural alterations including high electron dense in mitochondrial matrix and lipid accumulation were also observed. In addition, abundances of transcripts of Cu/Zn superoxide dismutase (SOD), phospholipid hydroperoxide glutathione peroxidase (PHGPx), and heat shock protein 90 (HSP) were decreased in larvae exposed to 60 and 150 μg L TCS, while transcript level of HSP was increased at 30 μg L TCS. Also, abundances of transcripts of acetyl-CoA carboxylase (ACC), carnitine palmitoyltransferase 2 (CPT2), peroxisome proliferator-activated receptor alpha (PPARa), fatty acid elongase 1 (FAE), sterol carrier protein 2 (SCP) were significantly lesser in larvae exposed to 60 and 150 μg L TCS. Overall, TCS at high levels induced histopathological changes in the liver of B. gargarizans tadpoles. This might have been due to the alteration of oxidative stress-related genes and lipid metabolism-related genes expression levels.
在本研究中，评估了 TCS 对中华大蟾蜍蝌蚪肝脏健康的不良影响。中华大蟾蜍幼虫从 Gosner 阶段 3 暴露于 0、10、30、60 和 150μg/L 的 TCS，直至变态高峰期。测定了肝体比（HSI）、肝组织学和超微结构特征，以及与解毒和氧化应激以及脂质代谢相关的基因在肝脏中的转录水平。暴露于 150μg/L TCS 导致变态高峰期蝌蚪的 HSI 增加。在 60 和 150μg/L TCS 下，肝脏中观察到黑色素巨噬细胞数量增加、核固缩和胶原纤维沉积等组织学变化。此外，还观察到明显的超微结构改变，包括线粒体基质中电子密度增加和脂质积累。此外，暴露于 60 和 150μg/L TCS 的幼虫中 Cu/Zn 超氧化物歧化酶（SOD）、磷脂氢过氧化物谷胱甘肽过氧化物酶（PHGPx）和热休克蛋白 90（HSP）的转录物丰度降低，而 HSP 的转录物丰度在 30μg/L TCS 时增加。此外，暴露于 60 和 150μg/L TCS 的幼虫中转录物丰度的乙酰辅酶 A 羧化酶（ACC）、肉碱棕榈酰基转移酶 2（CPT2）、过氧化物酶体增殖物激活受体 alpha（PPARa）、脂肪酸延长酶 1（FAE）、甾醇载体蛋白 2（SCP）显著减少。总之，高水平的 TCS 诱导了中华大蟾蜍蝌蚪肝脏的组织病理学变化。这可能是由于氧化应激相关基因和脂质代谢相关基因表达水平的改变。
