Transcriptome analysis reveals the different toxic mechanism of three HBCD diastereoisomers to Brachionus plicatilis based on chemical defensome.

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Tác giả: Yijun Li, Na Lu, Xiaocheng Wang, You Wang, Zhongyong Yan, Yaya Zhang

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: Netherlands : Journal of hazardous materials , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 701296

 The emerging contaminants hexabromocyclododecanes (HBCDs) are proved to exhibit highly reproductive toxicity to marine rotifer Brachionus plicatilis, but how about the toxic differentiation among three diastereoisomers of HBCD, and what's the possible hidden mechanism? B. plicatilis was exposed to different concentrations of HBCD diastereoisomers, and the results showed that α-, β- and γ-HBCD exhibited various toxicity on it, the adverse effects on individual life history traits included shortened lifespan, shortened body length and reduced offspring number. Population dynamics analysis showed that the maximum population density and time to reach it were also significantly influenced. The integrated biomarker responses (IBR) were constructed based on key life history traits and population dynamics indicators, and the comprehensive toxicity ranking of HBCD diastereoisomers was β-HBCD>
  α-HBCD>
  γ-HBCD, which was consistent with acute experimental results. Results of transcriptome with emphasis on chemical defensome was conducted. Genes including cytochrome P450 enzymes (CYP450s), aldehyde dehydrogenases (ALDHs), glutathione S-transferases (GSTs) and SOD were upregulated under γ-HBCD compared to those under α- and β-HBCD. Results of molecular docking suggested γ-HBCD had stronger affinity with aryl hydrocarbon receptor (AhR) that made it more easily activate the subsequent components of the defending pathway. Moreover, transcriptome result showed the level of autophagy, the newly found protective pathway in B. plicatilis was higher under α- and β-HBCD than that under γ-HBCD and the TEM observation result provided the consist directly proof. The chemical defensome and the subsequently autophagy seemed to be the hidden mechanism for the toxicity differentiation of the HBCD diastereoisomers.
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