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

• Published in: The Science of the total environment 2021-10, Vol.789, p.147989, Article 147989
• Main Authors: Elfawy, Hasnaa A., Anupriya, S, Mohanty, Swabhiman, Patel, Paritosh, Ghosal, Sayam, Panda, Pritam Kumar, Das, Biswadeep, Verma, Suresh K., Patnaik, Srinivas
• Format: Article
• Language: English
• Subjects: Benzo[a]pyrene; Bone-synthesis genes; Oxidative stress; Skeletal deformities; Zebrafish
• ISSN: 0048-9697; 1879-1026; 1879-1026
• DOI: 10.1016/j.scitotenv.2021.147989

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. [Display omitted] •BaP induced severe morphological and skeletal deformities in zebrafish embryos.•BaP delayed hatching rate by altering the hatching enzyme structure and function.•BaP accumulated primarily in the zebrafish embryonic yolk sac.•BaP induced down-regulation of expression of bone-related genes.•BaP specifically induced apoptosis in the head, backbone, and tail region of zebra fish.