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急性暴露于甲基汞对蠵龟红细胞的转录分析

Transcriptional Analyses of Acute Exposure to Methylmercury on Erythrocytes of Loggerhead Sea Turtle.

作者信息

Hernández-Fernández Javier, Pinzón-Velasco Andrés, López Ellie Anne, Rodríguez-Becerra Pilar, Mariño-Ramírez Leonardo

机构信息

Department of Natural and Environmental Science, Marine Biology Program, Faculty of Science and Engineering, Genetics, Molecular Biology and Bioinformatic Research Group-GENBIMOL, Jorge Tadeo Lozano University, Cra. 4 No 22-61, Bogotá 110311, Colombia.

Faculty of Sciences, Department of Biology, Pontificia Universidad Javeriana, Calle 45, Cra. 7, Bogotá 110231, Colombia.

出版信息

Toxics. 2021 Mar 29;9(4):70. doi: 10.3390/toxics9040070.

DOI:10.3390/toxics9040070
PMID:33805397
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8066450/
Abstract

To understand changes in enzyme activity and gene expression as biomarkers of exposure to methylmercury, we exposed loggerhead turtle erythrocytes (RBCs) to concentrations of 0, 1, and 5 mg L of MeHg and de novo transcriptome were assembled using RNA-seq. The analysis of differentially expressed genes (DEGs) indicated that 79 unique genes were dysregulated (39 upregulated and 44 downregulated genes). The results showed that MeHg altered gene expression patterns as a response to the cellular stress produced, reflected in cell cycle regulation, lysosomal activity, autophagy, calcium regulation, mitochondrial regulation, apoptosis, and regulation of transcription and translation. The analysis of DEGs showed a low response of the antioxidant machinery to MeHg, evidenced by the fact that genes of early response to oxidative stress were not dysregulated. The RBCs maintained a constitutive expression of proteins that represented a good part of the defense against reactive oxygen species (ROS) induced by MeHg.

摘要

为了解作为甲基汞暴露生物标志物的酶活性和基因表达变化，我们将蠵龟红细胞（RBC）暴露于0、1和5 mg/L的甲基汞浓度下，并使用RNA测序从头组装转录组。差异表达基因（DEG）分析表明，79个独特基因表达失调（39个上调基因和44个下调基因）。结果表明，甲基汞改变了基因表达模式，作为对所产生的细胞应激的反应，这反映在细胞周期调控、溶酶体活性、自噬、钙调节、线粒体调节、细胞凋亡以及转录和翻译调节中。DEG分析显示抗氧化机制对甲基汞的反应较低，这一事实证明，氧化应激早期反应的基因并未失调。红细胞维持了蛋白质的组成型表达，这些蛋白质构成了抵御甲基汞诱导的活性氧（ROS）的重要防御部分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/8da751ad3988/toxics-09-00070-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/e9e32f61f0a5/toxics-09-00070-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/ef2f76dc1263/toxics-09-00070-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/8dfd72ed7fc0/toxics-09-00070-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/43cbbe8b1e8c/toxics-09-00070-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/691747bb61bb/toxics-09-00070-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/db9c98935435/toxics-09-00070-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/73f63b1d5bde/toxics-09-00070-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/d5d940e15b84/toxics-09-00070-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/8da751ad3988/toxics-09-00070-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/e9e32f61f0a5/toxics-09-00070-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/ef2f76dc1263/toxics-09-00070-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/8dfd72ed7fc0/toxics-09-00070-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/43cbbe8b1e8c/toxics-09-00070-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/691747bb61bb/toxics-09-00070-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/db9c98935435/toxics-09-00070-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/73f63b1d5bde/toxics-09-00070-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/d5d940e15b84/toxics-09-00070-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68bd/8066450/8da751ad3988/toxics-09-00070-g009.jpg

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