Chronic exposure to bisphenol S is associated with antagonistic neurobehavioral transformation and cleaved caspase 3 induced neurodegeneration in zebrafish brain

IF 3.9 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Bhabani Sankar Sahoo , Lilesh Kumar Pradhan , Prerana Sarangi , Jayashree Digal , Suvam Bhoi , Pradyumna Kumar Sahoo , Sai Aparna , Sangeeta Raut , Saroj Kumar Das
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Abstract

Bisphenol S (BPS), a widely used bisphenol analogue, has been increasingly detected in aquatic environments, raising concerns about its potential neurotoxic effects. However, the mechanism underlying the neurotoxicity induced by BPS remains elusive. In this context, our present study was aimed to investigate the impact of temporal BPS exposure towards precocious development of neurobehavioral transformation and neurodegeneration in zebrafish brain. Heightened monoamine oxidase (MAO) activity is associated with induction of aggressive behavioural response. In line with earlier report, our findings following mirror biting test advocated that temporal BPS exposure is associated with gradual genesis of aggressive neurobehavioral response and is correlated with augmented MAO activity and downregulation of tyrosine hydroxylase (TH) expression in zebrafish brain. Our further observation towards native neurobehavioral response as regulated by periventricular grey zone (PGZ) of optic tectum (TeO) of brain showed that duration dependent exposure to BPS is associated with gross transformation in scototaxis and explorative behaviour of zebrafish. Concurrently, our objective was also predestined to emphasize the detrimental effect of BPS on brain biochemistry and neuromorphology. In this line, our findings showed that BPS-persuaded heightened oxidative stress is linked with augmented chromatin condensation and apoptotic cell death as depicted through cleaved caspase-3 expression in zebrafish brain. To understand neuromorphological integrity of PGZ region through expression of NeuN, our findings advocated a significant downregulation following temporal exposure to BPS. In a nutshell, the gross observation delineates the strong neurodegenerative potential of BPS coupled through neurobehavioral transformation, oxidative stress and neuromorphological alteration in zebrafish brain.

Abstract Image

慢性暴露于双酚S与斑马鱼大脑的拮抗神经行为转化和裂解型半胱天酶3诱导的神经变性有关。
双酚S (BPS)是一种广泛使用的双酚类似物,越来越多地在水生环境中被检测到,引起了人们对其潜在神经毒性作用的关注。然而,BPS引起神经毒性的机制尚不清楚。在此背景下,本研究旨在探讨时间BPS暴露对斑马鱼大脑神经行为转化和神经退行性变的早熟发育的影响。单胺氧化酶(MAO)活性升高与攻击性行为反应的诱导有关。与先前的报道一致,我们在镜像咬伤实验后的研究结果表明,暂时暴露于BPS与斑马鱼大脑中攻击性神经行为反应的逐渐发生有关,并与MAO活性增强和酪氨酸羟化酶(TH)表达下调有关。我们进一步观察了视神经顶盖(TeO)脑室周围灰区(PGZ)调节的天然神经行为反应,结果表明,持续暴露于BPS与斑马鱼的趋向性和探索行为的总体转变有关。同时,我们的目的也注定了强调BPS对脑生化和神经形态学的有害影响。在这条线上,我们的研究结果表明,bps诱导的氧化应激升高与染色质浓缩增强和凋亡细胞死亡有关,这是通过斑马鱼大脑中裂解的caspase-3表达来描述的。为了通过NeuN的表达了解PGZ区域的神经形态学完整性,我们的研究结果表明,在长时间暴露于BPS后,PGZ区域的NeuN表达显著下调。总而言之,总的观察描述了BPS在斑马鱼大脑中通过神经行为转化、氧化应激和神经形态学改变耦合的强大的神经退行性潜能。
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来源期刊
CiteScore
7.50
自引率
5.10%
发文量
206
审稿时长
30 days
期刊介绍: Part C: Toxicology and Pharmacology. This journal is concerned with chemical and drug action at different levels of organization, biotransformation of xenobiotics, mechanisms of toxicity, including reactive oxygen species and carcinogenesis, endocrine disruptors, natural products chemistry, and signal transduction with a molecular approach to these fields.
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