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甲萘醌诱导的氧化应激重塑了黄曲霉的氧化脂质谱及其生活方式。

Menadione-Induced Oxidative Stress Re-Shapes the Oxylipin Profile of Aspergillus flavus and Its Lifestyle.

作者信息

Zaccaria Marco, Ludovici Matteo, Sanzani Simona Marianna, Ippolito Antonio, Cigliano Riccardo Aiese, Sanseverino Walter, Scarpari Marzia, Scala Valeria, Fanelli Corrado, Reverberi Massimo

机构信息

Department of Environmental Biology, University of Rome Sapienza, Largo Cristina di Svezia 24, Rome 00165, Italy.

Department of Soil, Plant and Food Sciences, University of Bari Aldo Moro, Via Giovanni Amendola 165/A, Bari 70126, Italy.

出版信息

Toxins (Basel). 2015 Oct 23;7(10):4315-29. doi: 10.3390/toxins7104315.

DOI:10.3390/toxins7104315
PMID:26512693
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4626736/
Abstract

Aspergillus flavus is an efficient producer of mycotoxins, particularly aflatoxin B₁, probably the most hepatocarcinogenic naturally-occurring compound. Although the inducing agents of toxin synthesis are not unanimously identified, there is evidence that oxidative stress is one of the main actors in play. In our study, we use menadione, a quinone extensively implemented in studies on ROS response in animal cells, for causing stress to A. flavus. For uncovering the molecular determinants that drive A. flavus in challenging oxidative stress conditions, we have evaluated a wide spectrum of several different parameters, ranging from metabolic (ROS and oxylipin profile) to transcriptional analysis (RNA-seq). There emerges a scenario in which A. flavus activates several metabolic processes under oxidative stress conditions for limiting the ROS-associated detrimental effects, as well as for triggering adaptive and escape strategies.

摘要

黄曲霉是一种高效的霉菌毒素产生菌,尤其是黄曲霉毒素B₁,它可能是最具肝癌致癌性的天然化合物。尽管毒素合成的诱导因子尚未得到一致确认,但有证据表明氧化应激是其中的主要因素之一。在我们的研究中,我们使用甲萘醌,一种在动物细胞ROS反应研究中广泛应用的醌类物质,对黄曲霉施加应激。为了揭示在具有挑战性的氧化应激条件下驱动黄曲霉的分子决定因素,我们评估了从代谢(ROS和氧化脂质谱)到转录分析(RNA测序)等广泛的多种不同参数。结果呈现出这样一种情况,即黄曲霉在氧化应激条件下激活多个代谢过程,以限制与ROS相关的有害影响,并触发适应性和逃避策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2580/4626736/76441ddcbafa/toxins-07-04315-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2580/4626736/d44dbe1b66fd/toxins-07-04315-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2580/4626736/42eee8d991cb/toxins-07-04315-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2580/4626736/58eec9c6bb87/toxins-07-04315-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2580/4626736/dd05e01c05d5/toxins-07-04315-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2580/4626736/76441ddcbafa/toxins-07-04315-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2580/4626736/d44dbe1b66fd/toxins-07-04315-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2580/4626736/42eee8d991cb/toxins-07-04315-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2580/4626736/58eec9c6bb87/toxins-07-04315-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2580/4626736/dd05e01c05d5/toxins-07-04315-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2580/4626736/76441ddcbafa/toxins-07-04315-g005.jpg

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