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The effects of chronic cadmium exposure on Bufo gargarizans larvae: Histopathological impairment, gene expression alteration and fatty acid metabolism disorder in the liver.
Aquatic Toxicology ( IF 4.5 ) Pub Date : 2020-03-18 , DOI: 10.1016/j.aquatox.2020.105470
Zongqi Ju 1 , Jing Ya 1 , Xinyi Li 1 , Hongyuan Wang 1 , Hongfeng Zhao 1
Affiliation  

Cadmium (Cd) a highly toxic metal to human and wildlife health and it is hazardous to both terrestrial and aquatic life. In this study, we used RNA sequencing analysis to examine the effects of chronic cadmium exposure on liver lipid metabolism of Bufo gargarizans larvae. Tadpoles were exposed to cadmium concentrations at 0, 5, 10, 50, 100 and 200 μg L-1 from Gosner stage 26-42 of metamorphic climax. The results showed high dose cadmium (50, 100 and 200 μg L-1) caused obvious histological changes characterized by hepatocytes deformation, nuclear pyknosis, increasing melanomacrophage centers (MMCs) and aggregated lipid droplets. Moreover, transcriptome analysis showed that liver function was seriously affected by cadmium exposure. Furthermore, high dose cadmium significantly upregulated the mRNA expression of elongation of very-long-chain fatty acids 1 (ELOVL1), Mitochondrial trans-2-enoyl-CoA reductase (MECR), Trans-2, 3-enoyl-CoA reductase (TER) and Hydroxysteroid (17β) dehydrogenase type 12 (HSD17B12) which are related with fatty acid synthesis. Meanwhile, mRNA levels of genes related with fat acid oxidation such as acetyl-CoA acyltransferase 2 (ACAA2) and enoyl-coenzyme A (CoA) hydratase short chain 1 (ECHS1) were significantly upregulated while the expression of Acyl-coA thioesterase 1 (ACOT1), 3-hydroxyacyl-CoA dehydrogenase (HADH), Palmitoyl-protein thioesterase 1(PPT1) and Acetyl-CoA acyltransferase 1(ACAA1) was significantly downregulated by high dose cadmium exposure. Furthermore, the mRNA level of ATP-binding cassette subfamily B member 11 (ABCB11) related with bile secretion was significantly decreased exposed to high dose cadmium. Our results suggested cadmium can cause liver dysfunction by inducing histopathological damages, genetic expression alterations and fatty acid metabolism disorder.

中文翻译:

慢性镉暴露对中华蟾蜍幼虫的影响:肝脏的组织病理学损害,基因表达改变和脂肪酸代谢紊乱。

镉(Cd)对人类和野生生物健康具有剧毒,对陆生和水生生物均有害。在这项研究中,我们使用RNA测序分析来检查慢性镉暴露对中华蟾蜍幼虫肝脂质代谢的影响。从Gosner变质高潮阶段26-42开始,stage暴露于0、5、10、50、100和200μgL-1的镉浓度下。结果表明,高剂量的镉(50、100和200μgL-1)引起明显的组织学改变,其特征是肝细胞变形,核固缩,黑色素巨噬细胞中心(MMCs)增多和脂质滴聚集。此外,转录组分析表明,镉暴露严重影响肝功能。此外,高剂量镉显着上调了超长链脂肪酸1(ELOVL1),线粒体反式-2-烯酰辅酶A还原酶(MECR),反式2、3-烯酰辅酶A还原酶(TER)和与脂肪酸合成有关的12型羟类固醇(17β)脱氢酶(HSD17B12)。同时,与脂肪酸氧化相关的基因,例如乙酰辅酶A酰基转移酶2(ACAA2)和烯酰辅酶A(CoA)水合酶短链1(ECHS1)的mRNA水平显着上调,而酰基辅酶A硫酯酶1(ACOT1) ),高剂量镉暴露显着下调了3-羟酰基辅酶A脱氢酶(HADH),棕榈酰蛋白硫酯酶1(PPT1)和乙酰辅酶A酰基转移酶1(ACAA1)。此外,高剂量镉暴露后,与胆汁分泌有关的ATP结合盒B亚家族成员11(ABCB11)的mRNA水平显着降低。我们的结果表明,镉可通过诱导组织病理学损害,基因表达改变和脂肪酸代谢紊乱而引起肝功能障碍。
更新日期:2020-03-19
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