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蛋鸡肝脏短期暴露于黄曲霉毒素B1时谷胱甘肽氧化还原系统的调节和活性变化以及脂质过氧化过程

Changes in the regulation and activity of glutathione redox system, and lipid peroxidation processes in short-term aflatoxin B1 exposure in liver of laying hens.

作者信息

Erdélyi M, Balogh K, Pelyhe C, Kövesi B, Nakade M, Zándoki E, Mézes M, Kovács B

机构信息

Faculty of Agricultural and Environmental Sciences, Department of Nutrition, Szent István University, Gödöllő, Hungary.

MTA-KE Mycotoxins in the Food Chain Research Group, Kaposvár University, Kaposvár, Hungary.

出版信息

J Anim Physiol Anim Nutr (Berl). 2018 Aug;102(4):947-952. doi: 10.1111/jpn.12896. Epub 2018 Mar 31.

DOI:10.1111/jpn.12896
PMID:29604131
Abstract

The purpose of this study was to investigate the short-term (48 hr) effects of feeding aflatoxin contaminated diet (170.3 μg/kg AFB1) in 49-week-old laying hens. Liver samples were taken at 12-hr intervals. Feed intake, body weight, absolute and relative liver weight were the same in groups. However, there was no feed intake during both dark periods (between 12nd to 24th and 36th to 48th hours of the experiment); therefore, aflatoxin intake was also negligible. Markers of initial phase of lipid peroxidation, conjugated dienes and trienes did not change as effect of aflatoxin, but terminal marker, malondialdehyde content was significantly higher at 12 hr as effect of aflatoxin. No significant difference was found in reduced glutathione concentration and glutathione peroxidase activity between the groups. Expression of glutathione peroxidase 4 gene (GPX4) was significantly reduced due to aflatoxin treatment at 12 and 24 hr, but induced later, while glutathione reductase gene (GSR) expression was significantly lower at 24 hr and glutathione synthetase gene (GSS) in aflatoxin-treated group at 12 hr. The results suggest that aflatoxin induced oxygen-free radical formation, but it did not reach critical level during this short period of time to cause activation of the expression of glutathione system.

摘要

本研究的目的是调查给49周龄蛋鸡饲喂黄曲霉毒素污染日粮(170.3μg/kg AFB1)的短期(48小时)影响。每隔12小时采集肝脏样本。各组的采食量、体重、绝对和相对肝脏重量相同。然而,在两个黑暗期(实验的第12至24小时和第36至48小时)均无采食量;因此,黄曲霉毒素摄入量也可忽略不计。脂质过氧化初始阶段的标志物共轭二烯和三烯并未因黄曲霉毒素的作用而改变,但终末标志物丙二醛含量在12小时时因黄曲霉毒素的作用而显著升高。各组之间还原型谷胱甘肽浓度和谷胱甘肽过氧化物酶活性未发现显著差异。谷胱甘肽过氧化物酶4基因(GPX4)的表达在12小时和24小时时因黄曲霉毒素处理而显著降低,但随后诱导升高,而谷胱甘肽还原酶基因(GSR)的表达在24小时时显著降低,谷胱甘肽合成酶基因(GSS)在黄曲霉毒素处理组12小时时表达降低。结果表明,黄曲霉毒素诱导了氧自由基的形成,但在这段短时间内未达到导致谷胱甘肽系统表达激活的临界水平。

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