Developmental and Neurotoxicity of Acrylamide to Zebrafish

Park, Jong‐Su; Samanta, Palas; Lee, Sang‐Woo; Lee, Jieon; Cho, Jae-Woo; Chun, Hang-Suk; Yoon, Seokjoo; Kim, Woo‐Keun

doi:10.3390/ijms22073518

Cited by 39 publications

(18 citation statements)

References 41 publications

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“…The behavioral phenomics alterations indicated that life-cycle exposure to acrylamide can inactivate the neurobehavior of zebrafish, and increase the risk of anxiety, reduce the ability to adapt to the unfamiliar environment, and alter the instinctual behavior of zebrafish preference for the group. To unravel intrinsic mechanism, acrylamide may lead to neurotoxic effects in zebrafish, like the dysregulation of genes related to microtubules and presynaptic vesicle alteration ( 65 ). Although previous study evidenced acrylamide-treated zebrafish exhibited “depressive-like” phenotype comorbid with anxiety behavior due to acute neurotoxicity ( 18 ), we first showed that chronic acrylamide exposure exhibits anxiety symptoms and social disability, and weakens adaptability to the new environment.…”

Section: Discussionmentioning

confidence: 99%

High fried food consumption impacts anxiety and depression due to lipid metabolism disturbance and neuroinflammation

Wang

Wan

Zhuang

et al. 2023

Proc. Natl. Acad. Sci. U.S.A.

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Western dietary patterns have been unfavorably linked with mental health. However, the long-term effects of habitual fried food consumption on anxiety and depression and underlying mechanisms remain unclear. Our population-based study with 140,728 people revealed that frequent fried food consumption, especially fried potato consumption, is strongly associated with 12% and 7% higher risk of anxiety and depression, respectively. The associations were more pronounced among male and younger consumers. Consistently, long-term exposure to acrylamide, a representative food processing contaminant in fried products, exacerbates scototaxis and thigmotaxis, and further impairs exploration ability and sociality of adult zebrafish, showing anxiety- and depressive-like behaviors. Moreover, treatment with acrylamide significantly down-regulates the gene expression of tjp2a related to the permeability of blood–brain barrier. Multiomics analysis showed that chronic exposure to acrylamide induces cerebral lipid metabolism disturbance and neuroinflammation. PPAR signaling pathway mediates acrylamide-induced lipid metabolism disorder in the brain of zebrafish. Especially, chronic exposure to acrylamide dysregulates sphingolipid and phospholipid metabolism, which plays important roles in the development of anxiety and depression symptoms. In addition, acrylamide promotes lipid peroxidation and oxidation stress, which participate in cerebral neuroinflammation. Acrylamide dramatically increases the markers of lipid peroxidation, including (±)5-HETE, 11(S)-HETE, 5-oxoETE, and up-regulates the expression of proinflammatory lipid mediators such as (±)12-HETE and 14(S)-HDHA, indicating elevated cerebral inflammatory status after chronic exposure to acrylamide. Together, these results both epidemiologically and mechanistically provide strong evidence to unravel the mechanism of acrylamide-triggered anxiety and depression, and highlight the significance of reducing fried food consumption for mental health.

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Section: Discussionmentioning

confidence: 99%

High fried food consumption impacts anxiety and depression due to lipid metabolism disturbance and neuroinflammation

Wang

Wan

Zhuang

et al. 2023

Proc. Natl. Acad. Sci. U.S.A.

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“…Current research suggests that BDNF can act as a key neuroprotective factor in neurodegenerative diseases (Lu, et al 2013), such as Parkinson's disease (Palasz, et al 2020), Alzheimer's disease (Amidfar, et al 2020), and Huntington's chorea (Zhou, et al 2021). Synapsin I (Syn1) is a major peripheral protein regulating the release of mature neuronal synaptic vesicles on the surface of synaptic vesicle cytoplasm (Park, et al 2021;Corradi, et al 2008). It is primarily expressed in the central and peripheral nervous systems and is associated with early neuronal development, synaptic growth and development, and regulation of neurotransmitter release.…”

Section: Discussionmentioning

confidence: 99%

“…Exposure to ACR in the population occurs through multiple pathways, with occupational populations in industrial production mainly through skin contact, while others are exposed through smoking (Mojska, et al 2016), drinking water (Backe, et al 2014), and food intake . In vivo and in vitro studies have shown that ACR can cause neurotoxicity, reproductive toxicity, genotoxicity, and carcinogenicity in animals, but only neurotoxicity has been found in humans to date (Xu, et al 2014;Park, et al 2021). After entering the body, ACR is distributed in various tissues of the human body.…”

Section: Introductionmentioning

confidence: 99%

Inhibiting the expression of PGK1 can improve the damage of nerve cells caused by acrylamide

Wang

Pan

et al. 2023

Preprint

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Recent studies have shown that phosphoglycerate kinase 1 (PGK1) may improve neurodegeneration. However, the role of PGK1 in acrylamide(ACR)-induced neuronal damage is not yet clear. In this study, SD rats were treated with 6 mg/kg and 18 mg/kg of ACR, and PC12 cells were treated with 1.25 mM and 2.5 mM of ACR, and PC12 cells were transfected with PGK1 siRNA. Behavioral responses and histopathological changes in the rats were monitored, and transmission electron microscopy was used to observe changes in neurons and internal organelles in the hippocampal tissues of the various groups. Western blot and RT-qPCR were used to detect changes in the expression of neuronal-related proteins BDNF, Syn1, Nrf2 signaling pathway-related proteins and PGK1 in the hippocampal tissues of the rats and PC12 cells. Immunohistochemistry and immunofluorescence were used to analyze PGK1 expression in the hippocampal tissues of the rats. The results showed that after ACR treatment, obvious hindlimb clasping effect was observed in rats, hippocampal tissue pathology occurred, neuronal boundaries became blurred, mitochondria swelled, and organelles became sparse. BDNF and Syn1 mRNA expression and protein levels decreased both in vivo and in vitro, while Nrf2 and PGK1 mRNA expression and protein levels increased both in vivo and in vitro. In PC12 cells, inhibition of PGK1 can alleviate cell damage, and increase the expression of BDNF and Syn1 while Nrf2 expression is suppressed. These results suggest that inhibiting the expression of PGK1 can protect nerve cell damage induced by ACR.

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“…Perfluorooctane sulfonate, 17β-estradiol, ethanol, and acrylamide are just some of the other substances for which zebrafish has been used as a model to assess DNT, ANT, and behavioral toxicity (Tal et al 2020 ; Catron et al 2019b ; Park et al 2021 ; Fitzgerald et al 2021 ). Neurotoxic effects in mammals of acrylamide (which induces apoptosis and demyelination) and ethanol (which affects neuronal proliferation, motor neuron survival, and optic nerve loss) were similarly assessed with the zebrafish model (Parng et al 2007 ; Park et al 2021 ). Another study shows how zebrafish estrogen pathways are homologous to those in rodents and humans.…”

Section: Nams and Neurotoxicity Assessmentmentioning

confidence: 99%

Recent advances and current challenges of new approach methodologies in developmental and adult neurotoxicity testing

Serafini,

Sepehri,

Midali

et al. 2024

Arch Toxicol

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Adult neurotoxicity (ANT) and developmental neurotoxicity (DNT) assessments aim to understand the adverse effects and underlying mechanisms of toxicants on the human nervous system. In recent years, there has been an increasing focus on the so-called new approach methodologies (NAMs). The Organization for Economic Co-operation and Development (OECD), together with European and American regulatory agencies, promote the use of validated alternative test systems, but to date, guidelines for regulatory DNT and ANT assessment rely primarily on classical animal testing. Alternative methods include both non-animal approaches and test systems on non-vertebrates (e.g., nematodes) or non-mammals (e.g., fish). Therefore, this review summarizes the recent advances of NAMs focusing on ANT and DNT and highlights the potential and current critical issues for the full implementation of these methods in the future. The status of the DNT in vitro battery (DNT IVB) is also reviewed as a first step of NAMs for the assessment of neurotoxicity in the regulatory context. Critical issues such as (i) the need for test batteries and method integration (from in silico and in vitro to in vivo alternatives, e.g., zebrafish, C. elegans) requiring interdisciplinarity to manage complexity, (ii) interlaboratory transferability, and (iii) the urgent need for method validation are discussed.

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Developmental and Neurotoxicity of Acrylamide to Zebrafish

Cited by 39 publications

References 41 publications

High fried food consumption impacts anxiety and depression due to lipid metabolism disturbance and neuroinflammation

High fried food consumption impacts anxiety and depression due to lipid metabolism disturbance and neuroinflammation

Inhibiting the expression of PGK1 can improve the damage of nerve cells caused by acrylamide

Recent advances and current challenges of new approach methodologies in developmental and adult neurotoxicity testing

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