Wu Chao, Zhang Yuhui, Chai Lihong, Wang Hongyuan
College of Life Science, Shaanxi Normal University, Xi'an 710119, China.
School of Environmental Science and Engineering, Chang'an University, Xi'an 710054, China; Key Laboratory of Subsurface Hydrology and Ecological Effect in Arid Region of Ministry of Education, Xi'an 710062, China.
Chemosphere. 2017 Jul;179:337-346. doi: 10.1016/j.chemosphere.2017.03.131. Epub 2017 Mar 31.
Chinese toad (Bufo gargarizans) were exposed to different concentrations of cadmium (5, 50, 100, 200 and 500 μg Cd L) from Gosner stage 3-42. Metamorphosis rate, body weight, total length and body length were measured. Histological alterations in thyroid gland and liver were examined. Changes in hepatocyte were also examined using Transmission electron microscopic. In addition, the mRNA expression of several genes involved in lipid metabolism, oxidative stress and thyroid hormones signaling pathways were also measured. Our results showed that 200 and 500 μg Cd L decreased the metamorphosis rate and inhibited the body size of B. gargarizans larvae at G42. Moreover, histological examinations have clearly exhibited that cadmium caused liver damage. Ultrastructural examination revealed lipid accumulation and abnormal mitochondria. Exposure to 200 and 500 μg Cd L significantly up-regulated mRNA expression of D2, SOD, GPx, ACC and FAE, but down-regulated mRNA expression of TRα, TRβ, PPARα, ACOX, CPT and SCP. However, low Cd concentration (5, 50 and 100) exposure did not cause any effect in genes expression. Thus, we conclude that high Cd concentrations could affect the normal processes of lipid metabolism though increasing lipid synthesis and reducing the ability of fatty acid β-oxidation, and disturb thyroid hormone pathways in liver, and induced oxidative stress. In addition, lipid metabolism might be regulated by THs. To our knowledge, the present study is the first to report the influence of cadmium on hepatic lipid metabolism in B. gargarizans and will greatly provide new insights into cadmium hepatotoxicity in amphibian.
从戈斯纳3-42期开始，将中华蟾蜍（Bufo gargarizans）暴露于不同浓度的镉（5、50、100、200和500μg Cd/L）中。测量变态率、体重、全长和体长。检查甲状腺和肝脏的组织学变化。还使用透射电子显微镜检查肝细胞的变化。此外，还测量了参与脂质代谢、氧化应激和甲状腺激素信号通路的几个基因的mRNA表达。我们的结果表明，200和500μg Cd/L降低了变态率，并抑制了42期中华蟾蜍幼虫的体型。此外，组织学检查清楚地表明镉会导致肝脏损伤。超微结构检查显示脂质积累和线粒体异常。暴露于200和500μg Cd/L显著上调了D2、SOD、GPx、ACC和FAE的mRNA表达，但下调了TRα、TRβ、PPARα、ACOX、CPT和SCP的mRNA表达。然而，低镉浓度（5、50和100）暴露对基因表达没有任何影响。因此，我们得出结论，高镉浓度可能通过增加脂质合成和降低脂肪酸β-氧化能力来影响脂质代谢的正常过程，扰乱肝脏中的甲状腺激素途径，并诱导氧化应激。此外，脂质代谢可能受甲状腺激素调节。据我们所知，本研究首次报道了镉对中华蟾蜍肝脏脂质代谢的影响，并将为两栖动物镉肝毒性提供新的见解。
