Long-term bisphenol S exposure induces fat accumulation in liver of adult male zebrafish (Danio rerio) and slows yolk lipid consumption in F1 offspring

Wang, Weiwei; Zhang, Xiaona; Qin, Jingyu; Wei, Penghao; Jia, Yonggang; Wang, Jun; Ru, Shaoguo

doi:10.1016/j.chemosphere.2019.01.020

Cited by 51 publications

(17 citation statements)

References 94 publications

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“…The down regulation of PPAR signaling in the zebrafish IL6-OE suggests that it might serve as an alternative to model NAFLD in humans. In a recently published study adult male zebrafish exposed to bisphenol S accumulate fat in the liver (34). This model also shows a down regulation of PPAR alpha expression.…”

Section: β -Oxidation and Autophagy In Il6-oe Male Livermentioning

confidence: 79%

Chronic systemic exposure to IL6 leads to deregulation of glycolysis and fat accumulation in the zebrafish liver

Singh

Jayarajan

Varshney

et al. 2021

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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Section: β -Oxidation and Autophagy In Il6-oe Male Livermentioning

confidence: 79%

Chronic systemic exposure to IL6 leads to deregulation of glycolysis and fat accumulation in the zebrafish liver

Singh

Jayarajan

Varshney

et al. 2021

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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“…BPS can enter the body in a variety of ways, such as through diet, skin contact, water input, and food-chain transmission. − BPS has been detected in surface water samples from major rivers in many countries at concentrations up to 7.2 μg/L. − The average BPS concentration in urine samples ( n = 315) in the United States and seven Asian countries is 0.654 ng/mL, and the concentration in serum samples ( n = 240) in China is 1.43 ng/mL . In mice and zebrafish, BPS causes a significant increase in plasma lipids, , which is a key precondition for atherosclerosis (AS) pathogenesis. Furthermore, low-dose BPS had a proarrhythmic impact on female rat hearts, similar to the risk of cardiovascular disease conferred by BPA .…”

Section: Introductionmentioning

confidence: 99%

Bisphenol S Induces Ectopic Angiogenesis in Embryos via VEGFR2 Signaling, Leading to Lipid Deposition in Blood Vessels of Larval Zebrafish

Wang

et al. 2020

Environ. Sci. Technol.

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Bisphenol S (BPS), used as a bisphenol A substitute, has been detected in various environments. However, the safety of BPS is still unclear. Here, zebrafish embryos were exposed to BPS (0, 1, 10, and 100 μg/L) for 24, 48, 72, 96 h, and 15 days. BPS induced ectopic sprouting of budding blood vessels in embryos, but the blood flow velocity within these lesions was unchanged at 48 h. At 72 h postfertilization (hpf), by observing the subintestinal venous plexus responsible for yolk absorption, we found that VEGFR2 transduced an angiogenic signal and that the subsequent reduction in blood flow velocity inhibited yolk absorption. At 96 hpf, yolk consumption was still delayed because of the disturbed transportation route, resulting in transient extensive lipid retention in the blood vessels. After feeding, obvious atherogenic lipids were discovered in the blood vessels, especially in bends, bifurcations, and stenoses. This dynamic visualization of the pathogenesis demonstrates a plausible mechanistic link between BPS exposure-induced embryonic vessel overgrowth and an increased atherosclerosis risk.

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“…If the liver is damaged, the absorption of yolk sac will be disturbed. Therefore, the absorption of yolk sac can also reflect the degree of liver injury (Sant and Timme-Laragy, 2018; Wang et al, 2019; Zhang et al, 2021). When the liver is seriously affected or chemicals induce hypertrophy or atrophy, the liver size may change (Zhang et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Transcriptome analysis reveals hepatotoxicity in zebrafish induced by cyhalofop-butyl

Zhou

Yang

Liu

2022

Preprint

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Cyhalofop-butyl is a highly effective aryloxyphenoxypropionate herbicide and widely used for weed control in paddy fields. With the increasing residue of herbicides, it poses a threat to the survival of aquatic organisms. Here, we evaluated the effect of cyhalofop-butyl on zebrafish to explore its potential hepatotoxic mechanism. The results showed that cyhalofop-butyl (0.1, 0.2 and 0.4 mg/L) induced hepatocyte degeneration, vacuolation and necrosis of larvae after embryonic exposure for 4 days and caused liver atrophy after exposure for 5 days. Meanwhile, the activities of enzymes related to liver function named alanine transaminase (ALT), aspartate transaminase (AST) were significantly increased by 0.2 mg/L cyhalofop-butyl and higher. And the contents of triglyceride (TG) involved in lipid metabolism was significantly decreased by 0.4 mg/L cyhalofop-buty. The effects of cyhalofop-butyl on zebrafish larvae were further demonstrated by GO (Gene Ontology) and KEGG pathway analysis. Cyhalofop-butyl (0.1, 0.2, 0.4 mg/L) altered the expression of 116, 154, 397 genes in liver,these genes are mainly enriched in metabolism (such as lipid metabolism, amino acid metabolism), immune system (Toll-like receptor signaling pathway) and endocrine system (PPAR signaling pathway). Furthermore, the expression of key genes related to liver development combined with RNA-Seq results, indicated that cyhalofop-butyl might damage the liver development of zebrafish larvae and cause metabolic disorders. To sum up, our research results reveal the physiological and molecular responses of zebrafish liver to cyhalofop-butyl and provide new insights for further studying the mechanism of cyhalofop-butyl toxicity to aquatic organisms.Graphical AbstractHighlightsCyhalofop-butyl induced liver damage of zebrafish larvae and caused liver atrophyCyhalofop-butyl affected liver function by increasing the activities of ALT and AST.Cyhalofop-butyl disturbed the lipid metabolism of liver in zebrafish via inhibition TG levels.Cyhalofop-butyl exposure induced metabolism and immune system disturbance at transcriptional levels.

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Long-term bisphenol S exposure induces fat accumulation in liver of adult male zebrafish (Danio rerio) and slows yolk lipid consumption in F1 offspring

Cited by 51 publications

References 94 publications

Chronic systemic exposure to IL6 leads to deregulation of glycolysis and fat accumulation in the zebrafish liver

Chronic systemic exposure to IL6 leads to deregulation of glycolysis and fat accumulation in the zebrafish liver

Bisphenol S Induces Ectopic Angiogenesis in Embryos via VEGFR2 Signaling, Leading to Lipid Deposition in Blood Vessels of Larval Zebrafish

Transcriptome analysis reveals hepatotoxicity in zebrafish induced by cyhalofop-butyl

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