Indole-3-acetic acid induced cardiogenesis impairment in in-vivo zebrafish via oxidative stress and downregulation of cardiac morphogenic factors

IF 4.2 3区 环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES Environmental toxicology and pharmacology Pub Date : 2024-05-29 DOI:10.1016/j.etap.2024.104479
S.P. Ramya Ranjan Nayak , Seenivasan Boopathi , Bader O. Almutairi , Selvaraj Arokiyaraj , M.K. Kathiravan , Jesu Arockiaraj
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Abstract

Plant growth regulators (PGRs) are increasingly used to promote sustainable agriculture, but their unregulated use raises concerns about potential environmental risks. Indole-3-acetic acid (IAA), a commonly used PGR, has been the subject of research on its developmental toxicity in the in-vivo zebrafish model. IAA exposure to zebrafish embryos caused oxidative stress, lipid peroxidation, and cellular apoptosis. The study also revealed that critical antioxidant genes including sod, cat, and bcl2 were downregulated, while pro-apoptotic genes such as bax and p53 were upregulated. IAA exposure also hampered normal cardiogenesis by downregulating myl7, amhc, and vmhc genes and potentially influencing zebrafish neurobehavior. The accumulation of IAA was confirmed by HPLC analysis of IAA-exposed zebrafish tissues. These findings underscore the need for further study on the potential ecological consequences of IAA use and the need for sustainable agricultural practices.

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吲哚-3-乙酸通过氧化应激和心脏形态形成因子的下调诱导体内斑马鱼心脏形成障碍。
植物生长调节剂(PGRs)越来越多地被用于促进可持续农业,但其无节制的使用引发了人们对潜在环境风险的担忧。吲哚-3-乙酸(IAA)是一种常用的植物生长调节剂,在体内斑马鱼模型中对其发育毒性进行了研究。斑马鱼胚胎接触 IAA 会导致氧化应激、脂质过氧化和细胞凋亡。研究还发现,sod、cat 和 bcl2 等关键抗氧化基因下调,而 bax 和 p53 等促凋亡基因上调。IAA暴露还通过下调myl7、amhc和vmhc基因阻碍了正常的心脏生成,并可能影响斑马鱼的神经行为。通过对暴露于IAA的斑马鱼组织进行高效液相色谱分析,证实了IAA的积累。这些发现强调了进一步研究使用IAA可能造成的生态后果的必要性以及可持续农业实践的必要性。
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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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