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日粮中赭曲霉毒素A对草鱼幼鱼生长性能和肠道顶端连接复合体的影响()。 (括号内内容原文缺失,翻译时保留原样)

Effects of Dietary Ochratoxin A on Growth Performance and Intestinal Apical Junctional Complex of Juvenile Grass Carp ().

作者信息

Liu Xin, Wu Pei, Jiang Wei-Dan, Liu Yang, Jiang Jun, Kuang Sheng-Yao, Tang Ling, Zhou Xiao-Qiu, Feng Lin

机构信息

Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, China.

Fish Nutrition and Safety Production University Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu 611130, China.

出版信息

Toxins (Basel). 2020 Dec 24;13(1):11. doi: 10.3390/toxins13010011.

Abstract

Ochratoxin A (OTA) contamination widely occurs in various feed ingredients and food crops, potentially posing a serious health threat to animals. In this research, 1260 juvenile grass carp were separately fed with seven distinct experimental diets (0, 406, 795, 1209, 1612, 2003 and 2406 µg of OTA/kg of diet) for 60 consecutive days to evaluate OTA's toxic effect on the intestinal apical junctional complex (including the tight junction (TJ) and the adherents junction (AJ)) and the underlying action mechanisms. Our experiment firstly confirmed that OTA caused fish growth retardation and disrupted the intestinal structural integrity. The detailed results show that OTA (1) depressed the feed efficiency, percentage weight gain and specific growth rate; (2) accumulated in the intestine; (3) caused oxidative damage and increased intestinal permeability; and (4) induced the RhoA/ROCK signaling pathway, destroying intestinal apical junctional complexes. Notably, OTA intervention did not result in changes in the gene expression of claudin-3c (in the proximal intestine (PI)), claudin-b and ZO-2b (in the mid intestine (MI) and distal intestine (DI)) in the fish intestine.

摘要

赭曲霉毒素A(OTA)污染广泛存在于各种饲料原料和粮食作物中,可能对动物健康构成严重威胁。在本研究中,1260尾草鱼幼鱼分别投喂七种不同的实验饲料(OTA含量分别为0、406、795、1209、1612、2003和2406 μg/kg饲料),连续投喂60天,以评估OTA对肠道顶端连接复合体(包括紧密连接(TJ)和黏附连接(AJ))的毒性作用及其潜在作用机制。我们的实验首先证实,OTA导致鱼类生长迟缓并破坏肠道结构完整性。具体结果表明,OTA(1)降低饲料效率、增重百分比和特定生长率;(2)在肠道中蓄积;(3)造成氧化损伤并增加肠道通透性;(4)诱导RhoA/ROCK信号通路,破坏肠道顶端连接复合体。值得注意的是,OTA干预并未导致草鱼肠道中claudin-3c(在近端肠道(PI)中)、claudin-b和ZO-2b(在中段肠道(MI)和远端肠道(DI)中)的基因表达发生变化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/992d/7823973/ea8f1f6ff2bf/toxins-13-00011-g001.jpg

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