Comparison of the impact of chlordecone and its metabolite chlordecol on genes involved in pesticide metabolism in HepG2 cell line

IF 4.2 3区环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES

Environmental toxicology and pharmacology Pub Date : 2025-04-17 DOI:10.1016/j.etap.2025.104701

Gulminyam Baratzhanova , Hanan EL Sheikh Saad , Agnès Fournier , Marion Huguet , Olivier Joubert , Arnaud Paul , Leyla Djansugurova , Céline Cakir-Kiefer

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引用次数: 0

Abstract

Chlordecone (CLD) is an organochlorine pesticide that is highly resistant in the environment. This compound and its metabolite chlordecol (CLD-OH) still can be found in the French West Indies, after being banned 30 years ago. The novelty of this work lies in evaluating the toxicity of CLD-OH compared to CLD and examining the effects of these compounds on nuclear receptor (PXR, PPARα, and CAR) and metabolism-related genes (CYP2B6, CYP3A4) in vitro using HepG2 cell line as a model. Our study demonstrates that both compounds displayed an almost similar pattern of decrease in cell viability. Moreover, it was shown that CLD-OH can increase the expression of PXR, CYP3A4, and PPARα genes in comparison to CLD. The AKR1C4 gene showed a slight decrease in expression after CLD treatment. Collectively, this study provided a new finding into the impact of CLD-OH and compares the mode of action of CLD and its metabolite.

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十氯酮及其代谢物氯醇对HepG2细胞株农药代谢相关基因影响的比较

十氯酮（CLD）是一种在环境中具有高度抗性的有机氯农药。这种化合物及其代谢物氯醇（CLD-OH）在30年前被禁止后，仍然可以在法属西印度群岛找到。这项工作的新颖之处在于，在体外以HepG2细胞系为模型，评估了CLD- oh与CLD相比的毒性，并研究了这些化合物对核受体（PXR， PPARα和CAR）和代谢相关基因（CYP2B6, CYP3A4）的影响。我们的研究表明，这两种化合物在细胞活力下降方面表现出几乎相似的模式。与CLD相比，CLD- oh可增加PXR、CYP3A4和PPARα基因的表达。AKR1C4基因在CLD处理后表达略有下降。总之，本研究对CLD- oh的影响提供了新的发现，并比较了CLD及其代谢物的作用方式。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Environmental toxicology and pharmacology 医学-毒理学

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.