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环境污染物暴露后,日本沼虾组织和人细胞中多功能免疫补体成分 1q(C1q)和凋亡相关基因的反应。

Responses of multifunctional immune complement component 1q (C1q) and apoptosis-related genes in Macrophthalmus japonicus tissues and human cells following exposure to environmental pollutants.

机构信息

Fisheries Science Institute, Chonnam National University, Yeosu, 59626, South Korea.

Department of Biotechnology, Chonnam National University, Yeosu, 59626, South Korea.

出版信息

Cell Stress Chaperones. 2023 Nov;28(6):959-968. doi: 10.1007/s12192-023-01389-y. Epub 2023 Oct 26.

DOI:10.1007/s12192-023-01389-y
PMID:37880562
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10746657/
Abstract

Apoptosis is a key defense process for multiple immune system functions, playing a central role in maintaining homeostasis and cell development. The purpose of this study was to evaluate the effects of environmental pollutant exposure on immune-related apoptotic pathways in crab tissues and human cells. To do this, we characterized the multifunctional immune complement component 1q (C1q) gene and analyzed C1q expression in Macrophthalmus japonicus crabs after exposure to di(2-ethylhexyl) phthalate (DEHP) or hexabromocyclododecanes (HBCDs). Moreover, the responses of apoptotic signal-related genes were observed in M. japonicus tissues and human cell lines (HEK293T and HCT116). C1q gene expression was downregulated in the gills and hepatopancreas of M. japonicus after exposure to DEHP or HBCD. Pollutant exposure also increased antioxidant enzyme activities and altered transcription of 15 apoptotic signaling genes in M. japonicus. However, patterns in apoptotic signaling in response to these pollutants differed in human cells. HBCD exposure generated an apoptotic signal (cleaved caspase-3) and inhibited cell growth in both cell lines, whereas DEHP exposure did not produce such a response. These results suggest that exposure to environmental pollutants induced different levels of immune-related apoptosis depending on the cell or tissue type and that this induction of apoptotic signaling may trigger an initiation of carcinogenesis in M. japonicus and in humans as consumers.

摘要

细胞凋亡是多种免疫系统功能的关键防御过程,在维持体内平衡和细胞发育方面发挥着核心作用。本研究旨在评估环境污染物暴露对蟹组织和人类细胞中与免疫相关的凋亡途径的影响。为此,我们对多功能免疫补体成分 1q(C1q)基因进行了特征描述,并分析了二(2-乙基己基)邻苯二甲酸酯(DEHP)或六溴环十二烷(HBCDs)暴露后日本沼虾(Macrothalmus japonicus)中 C1q 的表达。此外,还观察了日本沼虾组织和人细胞系(HEK293T 和 HCT116)中凋亡信号相关基因的反应。DEHP 或 HBCD 暴露后,日本沼虾的鳃和肝胰腺中 C1q 基因表达下调。污染物暴露还增加了日本沼虾中 15 种凋亡信号基因的转录和抗氧化酶活性。然而,这些污染物引起的凋亡信号在人类细胞中的反应模式不同。HBCD 暴露在两种细胞系中均产生凋亡信号(裂解的 caspase-3)并抑制细胞生长,而 DEHP 暴露则未产生这种反应。这些结果表明,暴露于环境污染物会根据细胞或组织类型引起不同程度的与免疫相关的细胞凋亡,并且这种凋亡信号的诱导可能会引发日本沼虾和人类作为消费者的致癌作用的发生。

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本文引用的文献

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Comp Biochem Physiol C Toxicol Pharmacol. 2022 Jul;257:109331. doi: 10.1016/j.cbpc.2022.109331. Epub 2022 Mar 25.
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Insight into microbial degradation of hexabromocyclododecane (HBCD) in lake sediments under different hydrodynamic conditions.在不同水动力条件下湖泊沉积物中六溴环十二烷(HBCD)微生物降解的研究进展。
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