Involvement of dopamine signaling pathway in neurodevelopmental toxicity induced by isoniazid in zebrafish

Liu, Li; Wu, Fang-yan; Zhu, Chengyue; Zou, Hong-yuan; Kong, Rui-qi; Ma, Yueming; Su, Dan; Song, Guoqiang; Zhang, Yun; Liu, Ke-chun

doi:10.1016/j.chemosphere.2020.129109

Cited by 19 publications

(9 citation statements)

References 40 publications

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“…In addition, stress-induced apoptosis alters the expression of bax (proapoptotic) and bcl-2 (antiapoptotic) genes, thereby affecting the mitochondrial release of cytochrome c (Meng et al, 2020). The ratio of bcl-2/bax transcription has been used as a determinant of apoptotic signals: A decrease in bcl-2/bax indicates cell death, whereas an increase in bcl-2/bax denotes apoptotic attenuation (Liu et al, 2021). Yuan et al (2019) reported that BPF and BPS induced apoptosis by increasing the transcription of bax and caspase-3 in zebrafish embryos.…”

Section: Discussionmentioning

confidence: 99%

“…Owing to the reported conserved molecular pathways between zebrafish and human (Howe et al, 2013), the zebrafish model has gained significant consideration as an in vivo tool used in assessing the toxicological profile of xenobiotics on a plethora of biological processes. For example, zebrafish was used to investigate the involvement of the dopamine signaling pathway in neurodevelopmental perturbations evoked by isoniazid (Liu et al, 2021). In the present study, we investigated oxidative stress and apoptosis as mediating mechanisms in evoking neurotoxicity of BPAF at a series of concentrations.…”

Section: Discussionmentioning

confidence: 99%

“…Extant literature supports the close association of developmental neurotoxicity with oxidative stress induced by reactive oxygen species (ROS; Liu et al, 2021;Nandi et al, 2019). An imbalance between the production of ROS and the antioxidant defense mechanism in a cell causes oxidative stress (Li et al, 2021), and this has been considered an early biomarker for xenobiotic-induced effects (Shehna Mahim et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

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Oxidative Stress and Apoptosis in Bisphenol AF–Induced Neurotoxicity in Zebrafish Embryos

Gyimah

Zhu

Zhang

et al. 2022

Enviro Toxic and Chemistry

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Bisphenol AF (BPAF) is a structural counterpart of bisphenol A that is utilized in the food and beverage industry.The present study investigated the potential mechanisms in BPAF-induced neurotoxicity in zebrafish embryos. The BPAF concentrations (0.03, 0.1, 0.3, and 1.0 µM) had no obvious effect on hatching, mortality, and body length of zebrafish larvae, while curved tail and pericardial edema were observed in the 1.0 μM group at 72 and 96 h postfertilization (hpf). Locomotor activity of the larvae (at 120 hpf) significantly decreased from dark to light but increased from light to dark transitions in BPAF groups (0.1, 0.3, and 1.0 μM). Acridine orange showed that BPAF significantly increased green fluorescence protein intensity (22.6%) in the 1.0 μM group. Consistently, the induced apoptosis significantly up-regulated caspase 3 at 0.3 μM (1.95-fold) and 1.0 μM (2.26-fold) and bax at 0.3 μM (1.60-fold) and 1.0 μM (1.78-fold), whereas bcl-2 expression was significantly decreased at 0.3 μM (0.72-fold) and 1.0 μM (0.53-fold). In addition, increased reactive oxygen species concentrations at 0.3 μM (27%) and 1.0 μM (61.4%) resulted in suppressed superoxide dismutase and catalase activities. Moreover, quantitative polymerase chain reaction results showed that BPAF (0.3 and 1.0 μM) significantly altered normal dopaminergic signaling where dat was up-regulated, while drd2a and th1 were down-regulated, in a concentration-dependent manner. Aberrations in dopamine-related genes were congruous with the dysregulations in neurodevelopment genes (sox11b, pax6a, syn2a, and rob2). Our findings suggest that BPAF-evoked oxidative stress and apoptosis could translate into phenotypical behavioral and neurodevelopmental abnormalities. These highlights could provide theoretical reference for risk assessment and act as an early indicator to BPAF exposure.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Oxidative Stress and Apoptosis in Bisphenol AF–Induced Neurotoxicity in Zebrafish Embryos

Gyimah

Zhu

Zhang

et al. 2022

Enviro Toxic and Chemistry

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“…Acriridine orange (AO) is a nucleic acid dye with unique spectral properties, which can penetrate and specifically label apoptotic cells, and emit green fluorescence ( Liu et al, 2021 ). Zebrafish embryos at 72 hpf were washed three times in embryo culture medium, treated with 4 mg/L AO and were incubated for 30 min in the dark.…”

Section: Methodsmentioning

confidence: 99%

Cyclosporine A Induces Cardiac Developmental Toxicity in Zebrafish by Up-Regulation of Wnt Signaling and Oxidative Stress

et al. 2021

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Due to the widely application of Cyclosporine A (CsA) as an immunosuppressant in clinic, it is necessary to study its potential toxicity. Therefore, we used zebrafish as a model animal to evaluate the toxicity of CsA on embryonic development. Exposure of zebrafish embryos to CsA at concentrations of 5 mg/L, 10 mg/L, and 15 mg/L from 12 hpf to 72 hpf resulted in abnormal embryonic development, including cardiac malformation, pericardial edema, decreased heart rate, decreased blood flow velocity, deposition at yolk sac, shortened body length, and increased distance between venous sinus and arterial bulb (SV-BA). The expression of genes related to cardiac development was disordered, and the apoptotic genes were up-regulated. Oxidative stress level was up-regulated and accumulated in pericardium in a dose-dependent manner. Astaxanthin (ATX) treatment could significantly alleviate zebrafish heart defects. CsA induced up-regulation of Wnt signaling in zebrafish, and IWR-1, an inhibitor of Wnt signaling pathway, could effectively rescue the heart defects induced by CsA. Together, our study indicated that CsA induced cardiac developmental toxicity in zebrafish larvae through up-regulating oxidative stress and Wnt signaling, contributing to a more comprehensive evaluation of the safety of the drug.

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“…All of them were provided by Key Laboratory for Drug Screening in Biology Institute, Qilu University of Technology (Shandong Academy of Sciences). Adult zebrafish were maintained at 28.0°C, on a 14/10‐h light/dark cycle under standard aquaculture conditions, as described before (L. Liu et al, 2021). Embryos were achieved through natural spawning.…”

Section: Methodsmentioning

confidence: 99%

Neurodevelopmental toxicity of pyrazinamide to larval zebrafish and the restoration after intoxication withdrawal

Wang

Zou

et al. 2022

J of Applied Toxicology

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To investigate the neurotoxicity of pyrazinamide (PZA) to larval zebrafish, the PZA effects were assessed followed by its mechanism being explored. Same as isoniazid (INH), this compound is a first-line anti-tuberculosis drug and is suggested to be a risk that inducing nerve injury with long-term intoxication. Our findings indicated that zebrafish larvae obtained severe nerve damage secondary to constant immersion in various concentrations of PZA (i.e., 0.5, 1.0, and 1.5 mM) from 4 hpf (hours post fertilization) onwards until 120 hpf. The damage presented as dramatically decrease of locomotor capacity and dopaminergic neuron (DAN)-rich region length in addition to defect of brain blood vessels (BBVs). Moreover, PZA-administrated zebrafish showed a decreased dopamine (DA) level and downregulated expression of neurodevelopment-related genes, such as shha, mbp, neurog1, and gfap. However, secondary to 48-h restoration in fish medium (i.e., at 168 hpf), the neurotoxicity described above was prominently ameliorated. The results showed that PZA at the concentrations we tested was notably neurotoxic to larval zebrafish, and this nerve injury was restorable after PZA withdrawing. Therefore, this finding will probably provide a reference for clinical medication.

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Involvement of dopamine signaling pathway in neurodevelopmental toxicity induced by isoniazid in zebrafish

Cited by 19 publications

References 40 publications

Oxidative Stress and Apoptosis in Bisphenol AF–Induced Neurotoxicity in Zebrafish Embryos

Oxidative Stress and Apoptosis in Bisphenol AF–Induced Neurotoxicity in Zebrafish Embryos

Cyclosporine A Induces Cardiac Developmental Toxicity in Zebrafish by Up-Regulation of Wnt Signaling and Oxidative Stress

Neurodevelopmental toxicity of pyrazinamide to larval zebrafish and the restoration after intoxication withdrawal

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