Pancreatic beta cells are a sensitive target of embryonic exposure to butylparaben in zebrafish (<i>Danio rerio</i>)

Brown, Sarah E.; Sant, Karilyn E.; Fleischman, Shana M.; Venezia, Olivia; Roy, Monika A.; Zhao, Ling; Timme‐Laragy, Alicia R.

doi:10.1002/bdr2.1215

Cited by 22 publications

(8 citation statements)

References 70 publications

(91 reference statements)

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“…We have previously demonstrated that the Islets of Langerhans are highly sensitive targets of toxicant exposures (Brown et al, 2018;Jacobs et al, 2018;Sant et al, 2016Sant et al, , 2017Timme-Laragy et al, 2015). In this study, we did not observe any significant changes in endocrine islet area, though we did observe increased incidence of islet morphological variants including fragmented islets.…”

Section: Discussioncontrasting

confidence: 54%

Perfluorobutanesulfonic Acid Disrupts Pancreatic Organogenesis and Regulation of Lipid Metabolism in the Zebrafish, Danio rerio

Sant

Venezia

Sinno

et al. 2018

Toxicological Sciences

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Since phase-out of highly persistent perfluorosulfonates in the U.S. from non-stick and stain-resistant products in the early 2000s, perfluorobutanesulfonic acid (PFBS) has replaced these compounds as a primary surfactant. Measurements of PFBS in environmental and human samples have been rising in recent years, raising concerns about potential negative health effects. We previously found that embryonic exposures to a related compound, perfluorooctanesulfonic acid (PFOS), decreased pancreas length and insulin-producing islet area in zebrafish embryos (Danio rerio). The objective of this study was to compare the effects of PFBS exposures on pancreatic organogenesis with our previous PFOS findings. Dechorionated zebrafish embryos from two different transgenic fish lines (Tg(insulin:GFP), Tg(ptf1a:GFP)) were exposed to 0 (0.01% DMSO), 16, or 32 µM PFBS daily beginning at 1 day post fertilization (dpf) until 4 and 7 dpf when they were examined using fluorescent microscopy for islet area and morphology, and exocrine pancreas length. PFBS-exposed embryos had significantly increased caudal fin deformities, delayed swim bladder inflation, and impaired yolk utilization. Incidence of fish with significantly stunted growth and truncated exocrine pancreas length was significantly increased, although these two effects occurred independently. Islet morphology revealed an increased incidence of severely hypomorphic islets (areas lower than the 1st percentile of controls) and an elevated occurrence of fragmented islets. RNA Seq data (4 dpf) also identify disruptions in regulation of lipid homeostasis. Overall, this work demonstrates that PFBS exposure can perturb embryonic development, energy homeostasis, and pancreatic organogenesis.

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Section: Discussioncontrasting

confidence: 54%

Perfluorobutanesulfonic Acid Disrupts Pancreatic Organogenesis and Regulation of Lipid Metabolism in the Zebrafish, Danio rerio

Sant

Venezia

Sinno

et al. 2018

Toxicological Sciences

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“…To date, studies on the effects of methyl and butylparaben on oxidative stress biomarkers in fish are still limited (e.g. Ateş et al, 2018;Brown et al, 2018) and for some parabens, such as ethyl, propyl and benzylparaben, the effects on antioxidant defenses are unknown.…”

Section: Introductionmentioning

confidence: 99%

Effects of parabens on antioxidant system and oxidative damages in Nile tilapia (Oreochromis niloticus)

Silva

Serrano

Oliveira

et al. 2018

Ecotoxicology and Environmental Safety

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In this study, effects of parabens on antioxidant defenses and oxidative damages in gills and liver of Nile tilapia (Oreochromis niloticus) were evaluated. Adult Nile tilapia were exposed to methyl, ethyl, propyl, butyl and benzylparaben and a mixture of methyl and propylparaben for 6 and 12 days. The biomarkers analyzed were superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), total glutathione (GSH-t) and lipid peroxidation measured by malondialdehyde (MDA) content. Results indicated that exposure to parabens caused biochemical changes in gill and liver cells, which in turn modulated enzymatic and non-enzymatic antioxidants in Nile tilapia. SOD, GPx and GR activity significantly increased in gills and liver after exposure to most parabens. CAT activity had little (liver) or no alteration (gills) in this fish species after treatment with parabens. GSH-t content in liver decreased after 6 days of exposure to parabens, but after 12 days, GSH-t levels increased in liver in all treatments, indicating an antioxidant adaptation to exposure to sublethal doses of parabens. Regarding the MDA levels, no alterations were observed in gills compared to control and in liver the MDA content was reduced after 12d of exposure to ethylparaben, butylparaben and paraben mixture, indicating no lipid peroxidation in the analyzed tissues. Our results demonstrate parabens-induced adaptive responses in fish, which were important in the protection against oxidative damages.

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“…While a direct mechanism of action between embryonic exposures to chemicals and the occurrence of diabetes later in life has not been confirmed, evidence suggests toxicants act to disrupt the sensitive developing pancreas via oxidative stress (Simmons, 2006). Developmental exposure to polychlorinated biphenyls, dioxins, phthalates, perfluorinated compounds, and various pharmaceuticals have been associated with diabetes in human epidemiological studies or associated with diabetic phenotypes, such as reduced beta‐cell mass, in animal models (Brown et al, 2018; Chen et al, 2014; Jacobs et al, 2018; Sant et al, 2016; Sant et al, 2019; Timme‐Laragy et al, 2015). Our study showed TCPMPOH is similarly capable of disrupting pancreatic organogenesis by reducing β cell mass and exocrine pancreas area.…”

Section: Discussionmentioning

confidence: 99%

“…For example, zebrafish exposed to perfluorooctanesulfonic acid (PFOS) had reduced beta cell area and pancreas length, as well as reduced gene expression of digestive enzymes and hormones governing glucoregulation (Sant, Jacobs, et al, 2017). Similar structural and transcriptional changes have been observed for other chemicals with endocrine activity, such as phthalates, perfluoroalkyl substances, parabens, and polychlorinated biphenyls (Brown et al, 2018;Chen et al, 2014;Sant et al, 2016;Sant, Venezia, Sinno, & Timme-Laragy, 2019;Timme-Laragy, Sant, Rousseau, & diIorio, 2015). Because many of these compounds disrupting pancreatic morphology are organohalogens, it is possible that TCPM and TCPMOH may exhibit similar behaviors during organogenesis.…”

Section: Introductionmentioning

confidence: 94%

Tris(4‐chlorophenyl)methane and tris(4‐chlorophenyl)methanol disrupt pancreatic organogenesis and gene expression in zebrafish embryos

Wilson

Cho

Allsing

et al. 2022

Birth Defects Research

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Objectives Tris(4‐chlorophenyl) methane (TCPM) and tris(4‐chlorophenyl)methanol (TCPMOH) are anthropogenic environmental contaminants believed to be manufacturing byproducts of the organochlorine pesticide dichlorodiphenyltrichloroethane (DDT) due to environmental co‐occurrence. TCPM and TCPMOH are persistent, bioaccumulate in the environment, and are detected in human breast milk and adipose tissues. DDT exposures have been previously shown to disrupt insulin signaling and glucoregulation, increasing risk for diabetes. We have previously shown that embryonic exposures organochlorines such as polychlorinated biphenyls disrupted pancreatic development and early embryonic glucoregulatory networks. Here, we determined the impacts of the similar compounds TCPM and TCPMOH on zebrafish pancreatic growth and gene expression following developmental exposures. Methods Zebrafish embryos were exposed to 50 nM TCPM or TCPMOH beginning at 24 hr postfertilization (hpf) and exposures were refreshed daily. At 96 hpf, pancreatic growth and islet area were directly visualized in Tg(ptf1a::GFP) and Tg(insulin::GFP) embryos, respectively, using microscopy. Gene expression was assessed at 100 hpf with RNA sequencing. Results Islet and total pancreas area were reduced by 20.8% and 13% in embryos exposed to 50 nM TCPMOH compared to controls. TCPM did not induce significant morphological changes to the developing pancreas, indicating TCPMOH, but not TCPM, impairs pancreatic development despite similarity in molecular responses. Transcriptomic responses to TCPM and TCPMOH were correlated (R2 = .903), and pathway analysis found downregulation of processes including retinol metabolism, circadian rhythm, and steroid biosynthesis. Conclusion Overall, our data suggest that TCPM and TCPMOH may be hazardous to embryonic growth and development.

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Pancreatic beta cells are a sensitive target of embryonic exposure to butylparaben in zebrafish (Danio rerio)

Abstract: The endocrine pancreas is a sensitive target of embryonic exposure to butylparaben, which also causes developmental deformities and perturbs redox conditions in the embryo.

Cited by 22 publications

References 70 publications

Perfluorobutanesulfonic Acid Disrupts Pancreatic Organogenesis and Regulation of Lipid Metabolism in the Zebrafish, Danio rerio

Perfluorobutanesulfonic Acid Disrupts Pancreatic Organogenesis and Regulation of Lipid Metabolism in the Zebrafish, Danio rerio

Effects of parabens on antioxidant system and oxidative damages in Nile tilapia (Oreochromis niloticus)

Tris(4‐chlorophenyl)methane and tris(4‐chlorophenyl)methanol disrupt pancreatic organogenesis and gene expression in zebrafish embryos

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