Zhang Caiying, Lin Tianjin, Nie Gaohui, Hu Ruiming, Pi Shaoxing, Wei Zejing, Wang Chang, Li Guyue, Hu Guoliang
Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang 330045, Jiangxi, PR China.
School of Information Technology,Jiangxi University of Finance and Economics, No. 665 Yuping West street, Economic and Technological Development District, Nanchang 330032, Jiangxi, PR China.
Ecotoxicol Environ Saf. 2022 Jan 15;230:113099. doi: 10.1016/j.ecoenv.2021.113099. Epub 2021 Dec 25.
Excess molybdenum (Mo) and cadmium (Cd) are widespread environmental and industrial metal pollutants. To evaluate the combined effects of Mo and Cd on calcium homeostasis and autophagy in duck kidneys. 160 healthy 7-day-old ducks (Anas platyrhyncha) were randomized into 4 groups and given to a basic diet, adding various doses of Mo or/and Cd for 16 weeks. On the 4th, 8th, 12th and 16th weeks, kidney tissues were collected. The study exhibited that Mo or/and Cd caused histological abnormality, reduced the activities of Ca ATPase, Mg ATPase, Na-K ATPase and Ca-Mg ATPase, K and Mg contents, and increased Na and Ca contents, upregulated CaMKKβ, CaMKIIɑ, CaN, IPR, GRP78, GRP94, CRT mRNA levels and CaMKIIɑ, CaN, IPR protein levels. Moreover, exposure to Mo or/and Cd notably promoted the amount of autophagosomes and LC3II immunofluorescence, upregulated AMPKα1, ATG5, Beclin-1, LC3A, LC3B mRNA levels and Beclin-1, LC3II/LC3I protein levels, downregulated mTOR, Dynein, P62 mRNA levels and P62 protein level. The changes of above indicators in combined group were more obvious. Overall, the results suggest that Mo and Cd co-exposure may can synergistically induce nephrotoxicity via causing calcium homeostasis disorder and autophagy in ducks.
过量的钼（Mo）和镉（Cd）是广泛存在的环境和工业金属污染物。为了评估钼和镉对鸭肾脏钙稳态和自噬的联合影响，将160只健康的7日龄鸭（绿头鸭）随机分为4组，给予基础日粮，并添加不同剂量的钼或/和镉，持续16周。在第4、8、12和16周时，采集肾脏组织。研究表明，钼或/和镉导致组织学异常，降低了钙ATP酶、镁ATP酶、钠钾ATP酶和钙镁ATP酶的活性、钾和镁含量，并增加了钠和钙含量，上调了钙调蛋白激酶β（CaMKKβ）、钙/钙调蛋白依赖性蛋白激酶Ⅱα（CaMKIIɑ）’钙调神经磷酸酶（CaN）、肌醇1,4,5-三磷酸受体（IPR）、葡萄糖调节蛋白78（GRP78）、葡萄糖调节蛋白94（GRP94）、钙网蛋白（CRT）的mRNA水平以及CaMKIIɑ、CaN、IPR的蛋白水平。此外，暴露于钼或/和镉显著增加了自噬体数量和LC3II免疫荧光，上调了腺苷酸活化蛋白激酶α1（AMPKα1）、自噬相关蛋白5（ATG5）、Beclin-1、微管相关蛋白轻链3A（LC3A）、微管相关蛋白轻链3B（LC3B）的mRNA水平以及Beclin-1、LC3II/LC3I的蛋白水平’下调了雷帕霉素靶蛋白（mTOR）、动力蛋白、P62的mRNA水平以及P62蛋白水平。联合组上述指标的变化更为明显。总体而言，结果表明钼和镉共同暴露可能通过导致鸭的钙稳态紊乱和自噬协同诱导肾毒性。
原文中“Mo and Cd co-exposure may can synergistically”存在语法错误，正确表述应为“Mo and Cd co-exposure may synergistically” ，译文已按正确理解翻译。
