Li Zhi-Hua, Chen Lu, Wu Yan-Hua, Li Ping, Li Yun-Feng, Ni Zhao-Hui
Key Laboratory of Freshwater Biodiversity Conservation (Ministry of Agriculture), Key Field Station for Fishery Resource and Environment in Upper-Middle Reaches of Yangtze River (Ministry of Agriculture), Yangtze River Fisheries Research Institute, Chinese Academy of Fishery Sciences, Wuhan 430223, China; University of South Bohemia in Ceske Budejovice, Faculty of Fisheries and Protection of Waters, South Bohemian Research Center of Aquaculture and Biodiversity of Hydrocenoses, Research Institute of Fish Culture and Hydrobiology, Zátiší 728/II, 389 25 Vodňany, Czech Republic.
Key Laboratory of Freshwater Biodiversity Conservation (Ministry of Agriculture), Key Field Station for Fishery Resource and Environment in Upper-Middle Reaches of Yangtze River (Ministry of Agriculture), Yangtze River Fisheries Research Institute, Chinese Academy of Fishery Sciences, Wuhan 430223, China.
Comp Biochem Physiol C Toxicol Pharmacol. 2014 Apr;161:53-7. doi: 10.1016/j.cbpc.2014.02.001. Epub 2014 Feb 9.
Cadmium is a heavy metal abundant in the environment that can induce endocrine disorder and toxicity in aquatic organisms at low levels. However, its effects on the thyroid system in fish are still unclear. In this study, the thyroid hormone (TH) levels and the expression profiles of genes related to hypothalamic- pituitary-thyroid (HPT) axis, including corticotropin-releasing hormone (crh), thyroid stimulating hormone beta (tshβ), solute carrier family 5 (sodium iodide symporter) member 5 (slc5a5), thyroglobulin (tg), thyroid hormone receptor alpha (trα) and thyroid hormone receptor beta (trβ), were determined in whole body of Chinese rare minnow (Gobiocypris rarus) larvae after exposure to different levels of Cd(2+) (0, 0.5 and 2.5mg/L) for 4days. And the 96-h lethal concentration of Cd(2+) on rare minnow larvae was determined as 2.59mg/L. The results showed that crh, slc5a5, tg and tshβ mRNA levels were significantly up-regulated in the larvae, but the gene expression of trα and trβ was down-regulated in a concentration-dependent manner. Besides, the THs levels decreased in the whole-body of fish, especially the thyroxine (T4) level. The above results indicated that Cd(2+) could alter gene expression in the HPT axis that might subsequently contribute to thyroid disruption.
镉是一种在环境中广泛存在的重金属，低浓度时就能导致水生生物出现内分泌紊乱和毒性。然而，其对鱼类甲状腺系统的影响仍不清楚。在本研究中，测定了暴露于不同浓度Cd²⁺（0、0.5和2.5mg/L）4天后中华稀有鮈鲫（Gobiocypris rarus）幼鱼全身的甲状腺激素（TH）水平以及与下丘脑 - 垂体 - 甲状腺（HPT）轴相关基因的表达谱，这些基因包括促肾上腺皮质激素释放激素（crh）、促甲状腺激素β（tshβ）、溶质载体家族5（钠碘同向转运体）成员5（slc5a5）、甲状腺球蛋白（tg）、甲状腺激素受体α（trα）和甲状腺激素受体β（trβ）。并且确定了Cd²⁺对稀有鮈鲫幼鱼的96小时致死浓度为2.59mg/L。结果显示，幼鱼体内crh、slc5a5、tg和tshβ的mRNA水平显著上调，但trα和trβ的基因表达呈浓度依赖性下调。此外，鱼体全身的TH水平下降，尤其是甲状腺素（T4）水平。上述结果表明，Cd²⁺可改变HPT轴中的基因表达，这可能随后导致甲状腺功能紊乱。
