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苯并(a)芘引发的氧化应激介导的分子毒性导致斑马鱼胚胎骨骼畸形和细胞凋亡。

Molecular toxicity of Benzo(a)pyrene mediated by elicited oxidative stress infer skeletal deformities and apoptosis in embryonic zebrafish.

作者信息

Elfawy Hasnaa A, Anupriya S, Mohanty Swabhiman, Patel Paritosh, Ghosal Sayam, Panda Pritam Kumar, Das Biswadeep, Verma Suresh K, Patnaik Srinivas

机构信息

School of Biotechnology, KIIT deemed to be University, Campus XI, Bhubaneswar, 751024, Odisha, India.

Condensed Matter Theory Group, Materials Theory Division, Department of Physics and Astronomy, Uppsala University, Sweden.

出版信息

Sci Total Environ. 2021 Oct 1;789:147989. doi: 10.1016/j.scitotenv.2021.147989. Epub 2021 May 24.

DOI:10.1016/j.scitotenv.2021.147989
PMID:34323819
Abstract

Benzo(a)pyrene (BaP) has become an integral component of disposed of plastic waste, organic pollutants, and remnants of combustible materials in the aquatic environment due to their persistent nature. The accumulation and integration of these polycyclic aromatic hydrocarbons (PAHs) have raised concern to human health and ecological safety. This study assessed the BaP-induced in vivo molecular toxicity with embryonic zebrafish inferred by oxidative stress and apoptosis. BaP was found to induce morphological and physiological abnormalities like delayed hatching (p < 0.05). Computational analysis demonstrated the high-affinity interaction of BaP with the zebrafish hatching enzyme (ZHE1) with Arg, Cys, Ala, Tyr, and Phe located at the active site revealing the influence of BaP on delayed hatching due to alteration of the enzyme structure. RT-PCR analysis revealed significant down-regulation of the skeletal genes Sox9a, SPP1/OPN, and Col1a1 (p < 0.05) genes. The cellular investigations unraveled that the toxicity of BaP extends to the skeletal regions of zebrafish (head, backbone, and tail) because of the elicited oxidative stress leading to apoptosis. The study extended the horizon of understanding of BaP toxicity at the molecular level which will enhance the indulgent and designing of techniques for better ecological sustainability.

摘要

由于其持久性,苯并(a)芘(BaP)已成为水环境中塑料垃圾、有机污染物和可燃材料残余物处理的一个组成部分。这些多环芳烃(PAHs)的积累和整合已引起对人类健康和生态安全的关注。本研究评估了BaP通过氧化应激和细胞凋亡对斑马鱼胚胎造成的体内分子毒性。发现BaP会诱导形态和生理异常,如孵化延迟(p < 0.05)。计算分析表明,BaP与斑马鱼孵化酶(ZHE1)具有高亲和力相互作用,活性位点处的精氨酸、半胱氨酸、丙氨酸、酪氨酸和苯丙氨酸揭示了BaP由于酶结构改变对孵化延迟的影响。逆转录聚合酶链反应(RT-PCR)分析显示,骨骼基因Sox9a、SPP1/OPN和Col1a1(p < 0.05)基因显著下调。细胞研究表明,由于引发氧化应激导致细胞凋亡,BaP的毒性扩展到斑马鱼的骨骼区域(头部、脊椎和尾部)。该研究扩展了在分子水平上对BaP毒性的理解范围,这将有助于更好地理解和设计实现更好生态可持续性的技术。

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