BDE-47 induced apoptosis in zebrafish embryos through mitochondrial ROS-mediated JNK signaling

Zhuang, Juan; Pan, Zhengjun; Mengqiu-Li,; Hong, Fashui; Zhu, Chuankun; Wu, Nan; Chang, Guoliang; Wang, Hui; Zhao, Xiangxiang

doi:10.1016/j.chemosphere.2020.127385

Cited by 44 publications

(27 citation statements)

References 65 publications

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“…As previously discussed for PS, this may reflect higher energetic cost linked to detoxification and ROS buffering responses, as robust BDE-47 induced oxidative stress has been reported in a variety of species including (developing) zebrafish (Fernie et al, 2005;Shao et al, 2008;Tagliaferri et al, 2010;Costa et al, 2015;Usenko et al, 2015;Meng et al, 2020;Messina et al, 2020). Again, similar to described PS mode of actions, BDE-47 and its hydroxylated metabolite 6-OH BDE-47, have recently been described to decrease mitochondrial OXPHOS gene expression and ATP production and increase oxygen consumption indicative of OXPHOS disruption uncoupling in zebrafish (Legradi et al, 2017;Zhuang et al, 2020), suggesting a mitochondrial contribution to the observed increase in oxygen consumption rate. Like PS, BDE-47 exposure also increased the feeding rate.…”

Section: Individual Ps Nanoplastic and Bde-47 Exposure Induces Organi...mentioning

confidence: 74%

Metabolic Consequences of Developmental Exposure to Polystyrene Nanoplastics, the Flame Retardant BDE-47 and Their Combination in Zebrafish

et al. 2022

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Single-use plastic production is higher now than ever before. Much of this plastic is released into aquatic environments, where it is eventually weathered into smaller nanoscale plastics. In addition to potential direct biological effects, nanoplastics may also modulate the biological effects of hydrophobic persistent organic legacy contaminants (POPs) that absorb to their surfaces. In this study, we test the hypothesis that developmental exposure (0–7 dpf) of zebrafish to the emerging contaminant polystyrene (PS) nanoplastics (⌀100 nm; 2.5 or 25 ppb), or to environmental levels of the legacy contaminant and flame retardant 2,2′,4,4′-Tetrabromodiphenyl ether (BDE-47; 10 ppt), disrupt organismal energy metabolism. We also test the hypothesis that co-exposure leads to increased metabolic disruption. The uptake of nanoplastics in developing zebrafish was validated using fluorescence microscopy. To address metabolic consequences at the organismal and molecular level, metabolic phenotyping assays and metabolic gene expression analysis were used. Both PS and BDE-47 affected organismal metabolism alone and in combination. Individually, PS and BDE-47 exposure increased feeding and oxygen consumption rates. PS exposure also elicited complex effects on locomotor behaviour with increased long-distance and decreased short-distance movements. Co-exposure of PS and BDE-47 significantly increased feeding and oxygen consumption rates compared to control and individual compounds alone, suggesting additive or synergistic effects on energy balance, which was further supported by reduced neutral lipid reserves. Conversely, molecular gene expression data pointed to a negative interaction, as co-exposure of high PS generally abolished the induction of gene expression in response to BDE-47. Our results demonstrate that co-exposure to emerging nanoplastic contaminants and legacy contaminants results in cumulative metabolic disruption in early development in a fish model relevant to eco- and human toxicology.

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Section: Individual Ps Nanoplastic and Bde-47 Exposure Induces Organi...mentioning

confidence: 74%

Metabolic Consequences of Developmental Exposure to Polystyrene Nanoplastics, the Flame Retardant BDE-47 and Their Combination in Zebrafish

et al. 2022

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“…The present study results are consistent with previous reports that BDE-47, 2, 6-dichlorobenzoquinone, 1,3,6,8-tetrabromocarbazole, HBCD, microcystin-LR, isoliquiritigenin, and induced developmental toxicity and apoptosis in zebrafish larvae/ embryos. [35][36][37][38][39][40][41] Previous studies also reported TCS caused caspase-8 and caspase-3 activation, DNA fragmentation and apoptotic body formation in neocortical neurons in vivo. 60 TCS affected axon formation in the neural development stages of zebrafish embryos.…”

Section: Discussionmentioning

confidence: 88%

“…34 Thus, zebrafish embryos/larvae have been extensively used in experiments to study the developmental toxicity of environmental pollutants. [35][36][37][38][39][40][41] To evaluate the ecological health risk of TCS and explore the molecular mechanism of TCS affecting apoptosis, the effect of developmental toxicity, oxidative stress, and apoptosis in zebrafish embryo-larvae exposed to environmentally relevant concentrations TCS was studied in the present study.…”

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confidence: 99%

Environmental relevant concentrations of triclosan affected developmental toxicity, oxidative stress, and apoptosis in zebrafish embryos

Liu

Zhang

Wang

2022

Environmental Toxicology

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Triclosan (TCS), as a broad-spectrum antibacterial agent, is widely used in various pharmaceutical and personal care products. However, the details of ecological environmental health risks of TCS are not clear. In this study, zebrafish embryos/ larval were exposed to environmentally relevant concentrations of TCS to evaluate the developmental toxicity. Four-hour post-fertilization (hpf) zebrafish embryos were exposed to 0, 2, 10, 50, and 250 μg/L TCS until 96 h. The heart beats at 72 hpf were significantly increased in 2 μg/L TCS group, while significantly decreased in 250 μg/L TCS treated group compared with control. The results of acridine orange staining, terminal deoxynucleotide transferase-mediated UTPnick end labeling assay, and detection of mitochondrial membrane potential showed that 50 and 250 μg/L TCS resulted in apoptosis. Meanwhile, reactive oxygen species (ROS) and DNA damage were induced, but SOD activity was significantly decreased in 250 μg/L TCS treated group. In addition, SOD(Mn) and GPx gene mRNA expressions were significantly down-regulated in 50 and 250 μg/L TCS treated groups, while Casp3, Casp9, Puma, Casp8, Apaf1, and Bid genes in 250 μg/L TCS and Mdm2 gene in 50 μg/L treated groups were significantly up-regulated. P53 protein was significantly up-regulated in 250 μg/L TCS treated group.The overall results showed that TCS can cause oxidative stress and result in apoptosis via the involvement of ROS-p53-caspase-dependent apoptotic pathway in zebrafish embryos. The present findings suggest the potential mechanisms of TCSinduced developmental toxicity appears to be the generation of ROS and the consequent triggering of apoptosis genes.

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Section: Introductionmentioning

confidence: 99%

“…In turn, JNK phosphorylation is promoted, and phosphorylated JNK further activate and promote the overexpression of the apoptosis proteins Bax, cysteinyl aspartate-speci c proteinase-3 (caspase-3), resulting in liver cell apoptosis, which can lead to liver degeneration and necrosis (Fig. 1) (6,8,9). Probiotics are a group of bioactive microorganisms that are bene cial to the host and improve its microecological balance and a favorable impact on the status and function of the intestinal tract (10,11).…”

Section: Introductionmentioning

confidence: 99%

Role and Mechanisms of Probiotics in Regulating the ROS/JNK Signaling Pathway in the Pathogenesis of Nonalcoholic Fatty Liver Disease.

Yang

Huang

et al. 2021

Preprint

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This study was aimed to investigate the impact of probiotics on regulating the ROS/JNK signaling pathway their underlying mechanism of action in the treatment of nonalcoholic fatty liver disease. For this purpose, male C57BL/6 mice were randomly divided into three groups: control, probiotics, and model groups. Methionine and choline deficiency (MCD) diets were fed for four weeks to establish a NAFLD mouse model. Serum levels of ALT, AST, TC, and TG were detected. Moreover, the pathological changes of the liver and ileum tissues were observed by hematoxylin and eosin (H&E) staining, and the content of reactive oxygen species (ROS) in liver tissues was determined. In addition, the levels of D-lactic acid and plasma and small intestine diamine oxidase were measured to evaluate the effects of probiotics on the intestinal tract of NAFLD mice. The expression levels of p-JNK, Bax, and Caspase-3 were established to analyze the regulatory mechanism of probiotics on the JNK signaling pathway. We found that probiotics improve liver function, repair intestinal barrier and significantly suppressed oxidative stress, JNK phosphorylation. Moreover, the application of probiotics regulated the expression of signaling pathway-related proteins and promoted the intestinal barrier function repair and decreased intestinal permeability. The data above suggest that probiotics alleviate NAFLD, whose mechanism might be associated with the regulation of ROS/JNK signaling pathway and the suppression of oxidative stress and apoptosis.

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BDE-47 induced apoptosis in zebrafish embryos through mitochondrial ROS-mediated JNK signaling

Cited by 44 publications

References 65 publications

Metabolic Consequences of Developmental Exposure to Polystyrene Nanoplastics, the Flame Retardant BDE-47 and Their Combination in Zebrafish

Metabolic Consequences of Developmental Exposure to Polystyrene Nanoplastics, the Flame Retardant BDE-47 and Their Combination in Zebrafish

Environmental relevant concentrations of triclosan affected developmental toxicity, oxidative stress, and apoptosis in zebrafish embryos

Role and Mechanisms of Probiotics in Regulating the ROS/JNK Signaling Pathway in the Pathogenesis of Nonalcoholic Fatty Liver Disease.

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