Modulating responses of indicator genes in cellular homeostasis, immune defense and apoptotic process in the Macrophthalmus japonicus exposed to di(2-ethylhexyl) phthalate as a plastic additive

IF 4.2 3区 环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES
Kiyun Park , Ihn-Sil Kwak
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引用次数: 0

Abstract

Di(2-ethylhexyl) phthalate (DEHP), have been increasingly used as plasticizers to manufacture soft and flexible materials and ubiquitously found in water and sediments in the aquatic ecosystem. The aim of the present study was to evaluate the effect of DEHP exposure on cellular homeostasis (HSF1 and seven HSPs), immune responses (ILF), and apoptotic responses (p53, BAX, Bcl-2). DEHP exposure upregulated the expression of HSF1 and ILF. Moreover, it altered the expression levels of HSPs (upregulation of HSP70, HSP90, HSP40, HSP83, and HSP67B2 and downregulation of HSP60 and HSP21) in conjunction with HSF1 and ILF in the gills and hepatopancreas of M. japonicus exposed to DEHP. At the protein level, DEHP exposure changed apoptotic signals in both tissues of M. japonicus. These findings indicate that chronic exposures to several DEHP concentrations could disturb cellular balance, damage the inflammatory and immune systems, and induce apoptotic cell death, thereby affecting the survival of M. japonicus.

调节暴露于作为塑料添加剂的邻苯二甲酸二(2-乙基己酯)的日本鲣鱼的细胞稳态、免疫防御和细胞凋亡过程中的指示基因的反应
邻苯二甲酸二(2-乙基己基)酯(DEHP)被越来越多地用作制造软性和柔性材料的增塑剂,并广泛存在于水生生态系统的水和沉积物中。本研究旨在评估接触 DEHP 对细胞稳态(HSF1 和七种 HSPs)、免疫反应(ILF)和凋亡反应(p53、BAX、Bcl-2)的影响。暴露于 DEHP 会上调 HSF1 和 ILF 的表达。此外,DEHP还改变了日本贻贝鳃和肝胰腺中HSPs的表达水平(HSP70、HSP90、HSP40、HSP83和HSP67B2上调,HSP60和HSP21下调)以及HSF1和ILF的表达水平。在蛋白质水平上,接触 DEHP 改变了日本贻贝两种组织中的凋亡信号。这些研究结果表明,长期暴露于多种浓度的DEHP会扰乱细胞平衡,破坏炎症和免疫系统,诱导细胞凋亡,从而影响日本贻贝的存活。
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来源期刊
CiteScore
7.00
自引率
4.70%
发文量
185
审稿时长
34 days
期刊介绍: Environmental Toxicology and Pharmacology publishes the results of studies concerning toxic and pharmacological effects of (human and veterinary) drugs and of environmental contaminants in animals and man. Areas of special interest are: molecular mechanisms of toxicity, biotransformation and toxicokinetics (including toxicokinetic modelling), molecular, biochemical and physiological mechanisms explaining differences in sensitivity between species and individuals, the characterisation of pathophysiological models and mechanisms involved in the development of effects and the identification of biological markers that can be used to study exposure and effects in man and animals. In addition to full length papers, short communications, full-length reviews and mini-reviews, Environmental Toxicology and Pharmacology will publish in depth assessments of special problem areas. The latter publications may exceed the length of a full length paper three to fourfold. A basic requirement is that the assessments are made under the auspices of international groups of leading experts in the fields concerned. The information examined may either consist of data that were already published, or of new data that were obtained within the framework of collaborative research programmes. Provision is also made for the acceptance of minireviews on (classes of) compounds, toxicities or mechanisms, debating recent advances in rapidly developing fields that fall within the scope of the journal.
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