A transcriptomics-based analysis provides insights into the sex-dependent reproductive toxicity of DEHP in zebrafish (Danio rerio)

IF 4.2 3区 环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES
Shirui Liu , Simeng Yu , Yankun Huang , Jingyun Zhang , Kai Song , Shenbao Qu , Cixin Li , Aijiang Yang , Xia Hu
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引用次数: 0

Abstract

Di-(2-ethylhexyl) phthalate (DEHP) threatens human and wildlife health seriously, yet sex-dependent reproductive toxicity remains unclear. Therefore, in this study, we exposed zebrafish to various concentrations (0.01, 0.1, 1.0, and 2.0 mg/L) of DEHP for 28 days. Results indicate that DEHP exposure induced oxidative stress as a common response in both sexes and more pronounced reproductive toxicity to males than females. In males, sperm development stagnated at spermatogonia and enriched pathways were mainly associated with ribosome (Rps3, Rps27a) and endoplasmic reticulum stress(Hspa5). In females, oocyte development was affected at later stages and the pathways were mainly lipid metabolism and GnRH signaling pathway. Hub genes from PPI in females were Cacna2d3, Prkcba, Calm2a, Pla2g4aa in SCvsHigh while Pla2g4aa in SCvsLow. Overall, these findings provide new insights into the molecular mechanisms of DEHP toxicity, which is crucial for understanding its impact on reproductive health and ecological risk assessment.
基于转录组学的分析为斑马鱼DEHP的性别依赖性生殖毒性提供了见解(Danio rerio)
邻苯二甲酸二-(2-乙基己基)酯(DEHP)严重威胁人类和野生动物的健康,但性别依赖性生殖毒性尚不清楚。因此,在本研究中,我们将斑马鱼暴露于不同浓度(0.01、0.1、1.0和2.0 mg/L)的DEHP中28天。结果表明,DEHP暴露诱导氧化应激是两性的共同反应,对男性的生殖毒性比女性更明显。男性精子发育停滞于精原细胞,其富集途径主要与核糖体(Rps3、Rps27a)和内质网应激(Hspa5)有关。在雌性中,卵母细胞发育在后期受到影响,其途径主要是脂质代谢和GnRH信号通路。雌性PPI中心基因为scvhigh中的Cacna2d3、Prkcba、Calm2a、Pla2g4aa和SCvsLow中的Pla2g4aa。总的来说,这些发现为DEHP毒性的分子机制提供了新的见解,这对于了解其对生殖健康和生态风险评估的影响至关重要。
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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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