Dietary Se deficiency dysregulates metabolic and cell death signaling in aggravating the AFB1 hepatotoxicity of chicks
Dietary Se deficiency dysregulates metabolic and cell death signaling in aggravating the AFB1 hepatotoxicity of chicks
复制标题
日粮硒缺乏调节代谢和细胞死亡信号，加剧雏鸡 AFB1 肝毒性
DOI：
10.1016/j.fct.2020.111938
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发表时间：
2021-01-12
影响因子：
4.3
通讯作者：
Sun，Lv-Hui
中科院分区：
文献类型：
--
作者：
Zhao，Ling;Deng，Jiang;Sun，Lv-Hui
本研究旨在利用iTRAQ蛋白质组学技术，系统分析黄曲霉毒素B1（AFB 1）对肉鸡肝脏的毒性作用机制及硒对其的保护作用。试验采用2 × 2析因设计，分别饲喂低硒日粮、低硒日粮+ 1.0 mg/kg黄曲霉毒素B_1、0.3 mg/kg硒和1.0 mg/kg黄曲霉毒素B_1 + 0.3 mg/kg硒，试验期3 wk。黄曲霉毒素B_1可使硒充足组血清ALT升高，总蛋白和白蛋白浓度降低，并引起肝组织病理学损害。值得注意的是，硒缺乏加剧了这些AFB 1诱导的变化。此外，硒缺乏降低肝谷胱甘肽过氧化物酶，但增加硫氧还蛋白还原酶和谷胱甘肽S-转移酶的活性和8-羟基脱氧鸟苷浓度在AFB 1组。此外，在硒充足和缺硒的日粮中，AFB 1共调控了261个差异表达蛋白（DEPs），而在AFB 1处理的日粮中，缺硒共调控了64个DEPs。这些DEPs主要与I、II相代谢酶、热休克蛋白、DNA修复、脂肪酸代谢和细胞凋亡有关。体外研究证实，醛酮还原酶家族1，member 10在黄曲霉毒素B1诱导的鸡来航雄肝癌细胞肝毒性和硒介导的黄曲霉毒素B1解毒中起重要作用。本研究分析了黄曲霉毒素B1和硒对肉鸡肝脏蛋白质组的影响，为黄曲霉毒素B1的肝毒性机制和硒的解毒机制提供了新的思路。
The objective of this study was to use isobaric tags for relative and absolute quantitation (iTRAQ) proteomic technology to systematically analyze the hepatotoxic mechanism of aflatoxin B1(AFB1) and its prevention by Se in broilers. Four groups of day-old broilers were allocated into a 2 × 2 factorial design trial that fed a Se-deficient based diet (BD) or the BD + 1.0 mg AFB1/kg, 0.3 mg Se/kg, or 1.0 mg AFB1/kg plus 0.3 mg Se/kg for 3 wk. Dietary AFB1increased serum ALT and decreased total protein and albumin concentrations, and induced hepatic histopathological lesions in Se adequate groups. Notably, Se deficiency exacerbated these AFB1-induced changes. Furthermore, Se deficiency reduced hepatic glutathione peroxidase but increased thioredoxin reductase and glutathione S-transferase activities and 8-hydroxydeoxyguanosine concentration in AFB1administrated groups. Moreover, AFB1dysregulated 261 co-differentially expressed proteins (DEPs) in both Se adequate and deficiency diets, and Se deficiency dysregulated 64 DEPs in AFB1administrated diets. These DEPs are mainly related to phase I and II metabolizing enzymes, heat shock proteins, DNA repair, fatty acid metabolism and apoptosis. Thein vitrostudy has verified that aldo-keto reductase family1, member10 plays an important role in AFB1-induced hepatotoxicity and Se-mediated detoxification of AFB1in a chicken leghorn male hepatoma cells. Conclusively, this study has analyzed the hepatic proteome response to dietary AFB1and Se, and thus shed new light on the mechanisms of hepatotoxicity of AFB1and its detoxification by Se in broilers.