Chronic exposure to bisphenol S induces oxidative stress, abnormal anxiety, and fear responses in adult zebrafish (Danio rerio)

Salahinejad, Arash; Attaran, Anoosha; Naderi, Mohammad; Meuthen, Denis; Niyogi, Som; Chivers, Douglas P.

doi:10.1016/j.scitotenv.2020.141633

Cited by 33 publications

(8 citation statements)

References 108 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, compared to the control group, relative expression of CAT, GPX, and ERβ1 was significantly decreased in all of the treated groups. Salahinejad et al evaluated the expression of CAT in zebrafish exposure to concentration-dependent groups of BPS, discovering the obviously down-regulated CAT expression [ 28 ], which was consistent with this study. It can be seen from Figure 4 a that the relative expression of CAT declined markedly with exposure time in the BPS treated group.…”

Section: Resultssupporting

confidence: 88%

Study on the Joint Toxicity of BPZ, BPS, BPC and BPF to Zebrafish

et al. 2021

View full text Add to dashboard Cite

Bisphenol Z (BPZ), bisphenol S (BPS), bisphenol C (BPC), and bisphenol F (BPF) had been widely used as alternatives to bisphenol A (BPA), but the toxicity data of these bisphenol analogues were very limited. In this study, the joint toxicity of BPZ, BPS, BPC, and BPF to zebrafish (Danio rerio) was investigated. The median half lethal concentrations (LC50) of BPZ, BPS, BPC, and BPF to zebrafish for 96 h were 6.9 × 105 µM, 3.9 × 107 µM, 7.1 × 105 µM, and1.6 × 106 µM, respectively. The joint toxicity effect of BPF–BPC (7.7 × 105–3.4 × 105µM) and BPZ–BPC (3.4 × 105–3.5 × 105µM) with the same toxic ratio showed a synergistic effect, which may be attributed to enzyme inhibition or induction theory. While the toxicity effect of the other two bisphenol analogue combined groups and multi-joint pairs showed an antagonistic effect due to the competition site, other causes need to be further explored. Meanwhile, the expression levels of the estrogen receptor genes (ERα, ERβ1) and antioxidant enzyme genes (SOD, CAT, GPX) were analyzed using a quantitative real-time polymerase chain reaction in zebrafish exposure to LC50 of BPZ, BPS, BPC, and BPF collected at 24, 48, 72, and 96 h. Relative expression of CAT, GPX, and ERβ1 mRNA declined significantly compared to the blank control, which might be a major cause of oxidant injury of antioxidant systems and the disruption of the endocrine systems in zebrafish.

show abstract

Section: Resultssupporting

confidence: 88%

Study on the Joint Toxicity of BPZ, BPS, BPC and BPF to Zebrafish

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Epidemiological survey indicated that prenatal exposure to BPA and BPS may affect child neurodevelopment [ 17 ]. Salahinejad et al found that chronic exposure to BPS affected cognitive behaviours in adult female zebrafish, with downregulation in the expression and activity of relevant genes and proteins involved in the glutamatergic–ERK–CREB (CAMP response element-binding protein) signalling cascade [ 18 ]. BPS affects the expression of 5α-reductase and the dopamine–serotonin system in the prefrontal cortex of infant female rats [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

The BDNF–TrkB–CREB Signalling Pathway Is Involved in Bisphenol S-Induced Neurotoxicity in Male Mice by Regulating Methylation

Zhu

et al. 2022

Toxics

View full text Add to dashboard Cite

Bisphenol S (BPS), the most common substitute for bisphenol A in manufacturing, is associated with neurotoxicity, but its molecular mechanisms are unclear. Here, we studied the role of the BDNF–TrkB–CREB (brain-derived neurotrophic factor–tropomyosin-related kinase B–CAMP response element-binding protein) signalling pathway in bisphenol S-induced neurotoxicity via methylation regulation in male C57BL/6 mice. The mice were treated with sesame oil or 2, 20 and 200 mg/kg body weight BPS for 28 consecutive days, and the hippocampus was extracted. We recorded the body weight, organ index, and hippocampal pathology and ultrastructure of the mice. The BDNF, TrkB, CREB, phosphorylated (p)-CREB, DNMTs (DNA methyltransferases) levels were determined by qRT-PCR and/or Western blotting. BDNF promoter IV methylation level was detected by bisulfite sequencing PCR. BPS damaged the mouse hippocampus ultrastructure and reduced the number of synapses. Further, it increased the methylation rate of BDNF promoter IV; downregulated BDNF, CREB, p-CREB/CREB and DNMT1 expression; and upregulated DNMT3a and DNMT3b expression. Therefore, we speculate that the BDNF–TrkB–CREB pathway may be involved in BPS-induced neurotoxicity in male mice by regulating methylation.

show abstract

“…10,27 Low-dose BPS treatment at 0.3 μM also alters certain behavioral parameters and mRNA levels of neurorelated genes in 5 dpf zebrafish, and BPS induced neurobehavioral disorder and disrupted the mRNA expression of enzymatic antioxidants in the brains of adult zebrafish at concentrations as low as 1 μg/L. 12,14,27 Therefore, BPS promotes ROS production and affects the development of the nervous system in the brain. However, the details of the mechanisms by which low-dose BPS exerts neurotoxicity remain unclear in vivo.…”

Section: Introductionmentioning

confidence: 99%

“…BPS is the main substitute for BPA, and the potential mechanisms underlying BPS-induced neurotoxicity have also been explored in several studies from the perspective of oxidative damage. Treatment with 1 nM to 100 μM BPS increases ROS levels and apoptosis rates in human neuroblastoma IMR-32 cells and induces apoptosis in male primary hippocampal neurons and hippocampal HT22 cells. ,, Recently, neurotoxicity tests in vivo revealed that BPS at high concentrations of 0.3 mg/L and 200 μg/L decreased locomotor behavior, promoted apoptosis, and inhibited central nervous system neurogenesis in zebrafish at 6 d postfertilization (dpf). , Low-dose BPS treatment at 0.3 μM also alters certain behavioral parameters and mRNA levels of neuro-related genes in 5 dpf zebrafish, and BPS induced neurobehavioral disorder and disrupted the mRNA expression of enzymatic antioxidants in the brains of adult zebrafish at concentrations as low as 1 μg/L. ,, Therefore, BPS promotes ROS production and affects the development of the nervous system in the brain. However, the details of the mechanisms by which low-dose BPS exerts neurotoxicity remain unclear in vivo .…”

Section: Introductionmentioning

confidence: 99%

Bisphenol S Impairs Behaviors through Disturbing Endoplasmic Reticulum Function and Reducing Lipid Levels in the Brain of Zebrafish

Wang

Zhang

et al. 2022

Environ. Sci. Technol.

View full text Add to dashboard Cite

The number of neurotoxic pollutants is increasing, but their mechanism of action is unclear. Here, zebrafish were exposed to 0, 1, 10, and 100 μg/L bisphenol S (BPS) for different durations beginning at 2 h postfertilization (hpf) to explore the neurotoxic mechanisms of BPS. Zebrafish larvae exposed to BPS displayed abnormal neurobehaviors. At 48 and 120 hpf, BPS inhibited yolk lipid consumption and reduced the lipid distribution in the zebrafish brain. Moreover, BPS downregulated the mRNA levels of genes involved in fatty acid elongation in the endoplasmic reticulum (ER) and activated ER stress pathways at 48 and 120 hpf, and KEGG analysis after RNA-seq showed that the protein processing pathway in the ER was significantly enriched after BPS exposure. Exposure to ER toxicants (thapsigargin and tunicamycin), two positive controls, induced neurotoxic effects on zebrafish embryos and larvae similar to those of BPS exposure. These data suggested that BPS and ER toxicants disturbed ER function and reduced brain lipid levels. Continued exposure to BPS into adulthood not only inhibited brain fatty acid elongation and ER function but also caused abnormal swelling of the ER in zebrafish. Our data provide new insights into the neurotoxic mechanism of BPS.

show abstract

Chronic exposure to bisphenol S induces oxidative stress, abnormal anxiety, and fear responses in adult zebrafish (Danio rerio)

Cited by 33 publications

References 108 publications

Study on the Joint Toxicity of BPZ, BPS, BPC and BPF to Zebrafish

Study on the Joint Toxicity of BPZ, BPS, BPC and BPF to Zebrafish

The BDNF–TrkB–CREB Signalling Pathway Is Involved in Bisphenol S-Induced Neurotoxicity in Male Mice by Regulating Methylation

Bisphenol S Impairs Behaviors through Disturbing Endoplasmic Reticulum Function and Reducing Lipid Levels in the Brain of Zebrafish

Contact Info

Product

Resources

About