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  1. Article ; Online: Decabromodiphenyl ethane induces locomotion neurotoxicity and potential Alzheimer's disease risks through intensifying amyloid-beta deposition by inhibiting transthyretin/transthyretin-like proteins.

    Wang, Chen / Zeng, Lingjun / Li, Yeyong / Shi, Chongli / Peng, Yi / Pan, Ruolin / Huang, Mengyan / Wang, Susu / Zhang, Jin / Li, Hui

    Environment international

    2022  Volume 168, Page(s) 107482

    Abstract: As a major alternative to traditional brominated flame retardants (BFRs), decabromodiphenyl ethane (DBDPE) is widely used and has been commonly detected in various environmental media and organisms. Few previous studies have focused on DBDPE-induced ... ...

    Abstract As a major alternative to traditional brominated flame retardants (BFRs), decabromodiphenyl ethane (DBDPE) is widely used and has been commonly detected in various environmental media and organisms. Few previous studies have focused on DBDPE-induced locomotion neurotoxicity, and the exact molecular mechanisms and related health risks remain unclear. In this study, we first analyzed the locomotion indicators of nematodes following DBDPE exposure, demonstrated that DBDPE caused locomotion neurotoxicity, and identified that a series of the transthyretin (TTR)-like genes participated in the regulation of nematode motility by transcriptomic analysis, gene transcription validation and TTR-like mutant verification. Subsequently, this study demonstrated that DBDPE exacerbated amyloid-beta (Aβ) deposition by repressing TTR/TTR-like gene transcription based on Alzheimer's disease (AD) model nematodes and human SH-SY5Y cells following DBDPE exposure and further revealed that DBDPE reduced the binding between TTR and Aβ by competing with the strand G region sites on the TTR/TTR-like protein, ultimately exacerbating Aβ deposition and the risk of AD. In short, our study demonstrated that DBDPE induced locomotion neurotoxicity and potential AD risks through intensifying Aβ deposition by inhibiting TTR/TTR-like proteins, providing reference support for risk management and policy formulation related to DBDPE and similarly structured novel BFRs.
    Language English
    Publishing date 2022-08-18
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 554791-x
    ISSN 1873-6750 ; 0160-4120
    ISSN (online) 1873-6750
    ISSN 0160-4120
    DOI 10.1016/j.envint.2022.107482
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Review of the toxicity and potential molecular mechanisms of parental or successive exposure to environmental pollutants in the model organism Caenorhabditis elegans

    Li, Hui / Zeng, Lingjun / Wang, Chen / Shi, Chongli / Li, Yeyong / Peng, Yi / Chen, Haibo / Zhang, Jin / Cheng, Biao / Chen, Chao / Xiang, Minghui / Huang, Yuan

    Environmental pollution. 2022 Oct. 15, v. 311

    2022  

    Abstract: Environmental pollutants such as heavy metals, nano/microparticles, and organic compounds have been detected in a wide range of environmental media, causing long-term exposure in various organisms and even humans through breathing, contacting, ingestion, ...

    Abstract Environmental pollutants such as heavy metals, nano/microparticles, and organic compounds have been detected in a wide range of environmental media, causing long-term exposure in various organisms and even humans through breathing, contacting, ingestion, and other routes. Long-term exposure to environmental pollutants in organisms or humans promotes exposure of offspring to parental and environmental pollutants, and subsequently results in multiple biological defects in the offspring. This review dialectically summarizes and discusses the existing studies using Caenorhabditis elegans (C. elegans) as a model organism to explore the multi/transgenerational toxicity and potential underlying molecular mechanisms induced by environmental pollutants following parental or successive exposure patterns. Parental and successive exposure to environmental pollutants induces various biological defects in C. elegans across multiple generations, including multi/transgenerational developmental toxicity, neurotoxicity, reproductive toxicity, and metabolic disturbances, which may be transmitted to progeny through reactive oxygen species-induced damage, epigenetic mechanisms, insulin/insulin-like growth factor-1 signaling pathway. This review aims to arouse researchers’ interest in the multi/transgenerational toxicity of pollutants and hopes to explore the possible long-term effects of environmental pollutants on organisms and even humans, as well as to provide constructive suggestions for the safety and management of emerging alternatives.
    Keywords Caenorhabditis elegans ; chronic exposure ; developmental toxicity ; epigenetics ; neurotoxicity ; oxygen ; pollution ; progeny ; reproductive toxicology
    Language English
    Dates of publication 2022-1015
    Publishing place Elsevier Ltd
    Document type Article
    ZDB-ID 280652-6
    ISSN 1873-6424 ; 0013-9327 ; 0269-7491
    ISSN (online) 1873-6424
    ISSN 0013-9327 ; 0269-7491
    DOI 10.1016/j.envpol.2022.119927
    Database NAL-Catalogue (AGRICOLA)

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  3. Article: Decabromodiphenyl ethane induces locomotion neurotoxicity and potential Alzheimer’s disease risks through intensifying amyloid-beta deposition by inhibiting transthyretin/transthyretin-like proteins

    Wang, Chen / Zeng, Lingjun / Li, Yeyong / Shi, Chongli / Peng, Yi / Pan, Ruolin / Huang, Mengyan / Wang, Susu / Zhang, Jin / Li, Hui

    Environment international. 2022 Oct., v. 168

    2022  

    Abstract: As a major alternative to traditional brominated flame retardants (BFRs), decabromodiphenyl ethane (DBDPE) is widely used and has been commonly detected in various environmental media and organisms. Few previous studies have focused on DBDPE-induced ... ...

    Abstract As a major alternative to traditional brominated flame retardants (BFRs), decabromodiphenyl ethane (DBDPE) is widely used and has been commonly detected in various environmental media and organisms. Few previous studies have focused on DBDPE-induced locomotion neurotoxicity, and the exact molecular mechanisms and related health risks remain unclear. In this study, we first analyzed the locomotion indicators of nematodes following DBDPE exposure, demonstrated that DBDPE caused locomotion neurotoxicity, and identified that a series of the transthyretin (TTR)-like genes participated in the regulation of nematode motility by transcriptomic analysis, gene transcription validation and TTR-like mutant verification. Subsequently, this study demonstrated that DBDPE exacerbated amyloid-beta (Aβ) deposition by repressing TTR/TTR-like gene transcription based on Alzheimer’s disease (AD) model nematodes and human SH-SY5Y cells following DBDPE exposure and further revealed that DBDPE reduced the binding between TTR and Aβ by competing with the strand G region sites on the TTR/TTR-like protein, ultimately exacerbating Aβ deposition and the risk of AD. In short, our study demonstrated that DBDPE induced locomotion neurotoxicity and potential AD risks through intensifying Aβ deposition by inhibiting TTR/TTR-like proteins, providing reference support for risk management and policy formulation related to DBDPE and similarly structured novel BFRs.
    Keywords Nematoda ; bromination ; decabromodiphenyl ethane ; environment ; humans ; issues and policy ; locomotion ; mutants ; neurotoxicity ; prealbumin ; risk ; risk management ; transcription (genetics) ; transcriptomics
    Language English
    Dates of publication 2022-10
    Publishing place Elsevier Ltd
    Document type Article
    ZDB-ID 554791-x
    ISSN 1873-6750 ; 0160-4120
    ISSN (online) 1873-6750
    ISSN 0160-4120
    DOI 10.1016/j.envint.2022.107482
    Database NAL-Catalogue (AGRICOLA)

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  4. Article ; Online: Triphenyl phosphate induced reproductive toxicity through the JNK signaling pathway in Caenorhabditis elegans.

    Shi, Chongli / Wang, Chen / Zeng, Lingjun / Peng, Yi / Li, Yeyong / Hao, Haibin / Zheng, Yang / Chen, Chao / Chen, Haibo / Zhang, Jin / Xiang, Minghui / Huang, Yuan / Li, Hui

    Journal of hazardous materials

    2022  Volume 446, Page(s) 130643

    Abstract: Triphenyl phosphate (TPHP) is a widely used aryl organophosphate flame retardant (OPFR) that has attracted attention due to its frequent detection in the environment and living organisms. To date, the reproductive toxicity of TPHP has been investigated ... ...

    Abstract Triphenyl phosphate (TPHP) is a widely used aryl organophosphate flame retardant (OPFR) that has attracted attention due to its frequent detection in the environment and living organisms. To date, the reproductive toxicity of TPHP has been investigated in organisms, but its molecular mechanisms are not fully understood. Caenorhabditis elegans (C. elegans) is the ideal animal for the study of reproductive toxicity following environmental pollutants, with short generation times, intact reproductive structures, and hermaphroditic fertilization. This study aimed to explore the reproductive dysfunction and molecular mechanisms induced by TPHP exposure in C. elegans. Specifically, exposure to TPHP resulted in a reduction in the number of eggs laid and developing embryos in utero, an increase in the number of apoptotic gonadal cells, and germ cell cycle arrest. The JNK signaling pathway is a potential pathway inducing reproductive toxicity following TPHP exposure based on transcriptome sequencing (RNA-seq). Moreover, TPHP exposure induced down-regulation of vhp-1 and kgb-2 gene transcription levels, and the knockout of vhp-1 and kgb-2 in the mutant strains exhibited more severe toxicity in apoptotic gonad cells, embryos, and eggs developing in utero, suggesting that vhp-1 and kgb-2 genes play a crucial role in TPHP-induced reproductive toxicity. Our data provide convergent evidence showing that TPHP exposure results in reproductive dysfunction through the JNK signaling pathway and improve our understanding of the ecotoxicity and toxicological mechanisms of aryl-OPFRs.
    MeSH term(s) Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; MAP Kinase Signaling System ; Organophosphates/toxicity ; Flame Retardants/toxicity ; Flame Retardants/metabolism
    Chemical Substances triphenyl phosphate (YZE19Z66EA) ; Organophosphates ; Flame Retardants
    Language English
    Publishing date 2022-12-20
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1491302-1
    ISSN 1873-3336 ; 0304-3894
    ISSN (online) 1873-3336
    ISSN 0304-3894
    DOI 10.1016/j.jhazmat.2022.130643
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Review of the toxicity and potential molecular mechanisms of parental or successive exposure to environmental pollutants in the model organism Caenorhabditis elegans.

    Li, Hui / Zeng, Lingjun / Wang, Chen / Shi, Chongli / Li, Yeyong / Peng, Yi / Chen, Haibo / Zhang, Jin / Cheng, Biao / Chen, Chao / Xiang, Minghui / Huang, Yuan

    Environmental pollution (Barking, Essex : 1987)

    2022  Volume 311, Page(s) 119927

    Abstract: Environmental pollutants such as heavy metals, nano/microparticles, and organic compounds have been detected in a wide range of environmental media, causing long-term exposure in various organisms and even humans through breathing, contacting, ingestion, ...

    Abstract Environmental pollutants such as heavy metals, nano/microparticles, and organic compounds have been detected in a wide range of environmental media, causing long-term exposure in various organisms and even humans through breathing, contacting, ingestion, and other routes. Long-term exposure to environmental pollutants in organisms or humans promotes exposure of offspring to parental and environmental pollutants, and subsequently results in multiple biological defects in the offspring. This review dialectically summarizes and discusses the existing studies using Caenorhabditis elegans (C. elegans) as a model organism to explore the multi/transgenerational toxicity and potential underlying molecular mechanisms induced by environmental pollutants following parental or successive exposure patterns. Parental and successive exposure to environmental pollutants induces various biological defects in C. elegans across multiple generations, including multi/transgenerational developmental toxicity, neurotoxicity, reproductive toxicity, and metabolic disturbances, which may be transmitted to progeny through reactive oxygen species-induced damage, epigenetic mechanisms, insulin/insulin-like growth factor-1 signaling pathway. This review aims to arouse researchers' interest in the multi/transgenerational toxicity of pollutants and hopes to explore the possible long-term effects of environmental pollutants on organisms and even humans, as well as to provide constructive suggestions for the safety and management of emerging alternatives.
    MeSH term(s) Animals ; Caenorhabditis elegans ; Environmental Pollutants/toxicity ; Epigenesis, Genetic ; Humans ; Metals, Heavy/toxicity ; Reproduction
    Chemical Substances Environmental Pollutants ; Metals, Heavy
    Language English
    Publishing date 2022-08-12
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 280652-6
    ISSN 1873-6424 ; 0013-9327 ; 0269-7491
    ISSN (online) 1873-6424
    ISSN 0013-9327 ; 0269-7491
    DOI 10.1016/j.envpol.2022.119927
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Tris(1,3-dichloro-2-propyl) phosphate reduces longevity through a specific microRNA-mediated DAF-16/FoxO in an unconventional insulin/insulin-like growth factor‑1 signaling pathway

    Wang, Chen / Li, Yeyong / Zeng, Lingjun / Shi, Chongli / Peng, Yi / Li, Hui / Chen, Haibo / Yu, Jun / Zhang, Jin / Cheng, Biao / Pan, Ruolin / Wang, Xiaoli / Xiang, Minghui / Huang, Yuan / Liu, Yongdi

    Journal of hazardous materials. 2022 Mar. 05, v. 425

    2022  

    Abstract: Tris(1,3-dichloro-2-propyl) phosphate (TDCPP) has received concerns due to its frequent detection in environmental media and biological samples. Our previous study has indicated TDCPP reduced the lifespan of Caenorhabditis elegans (C. elegans) by ... ...

    Abstract Tris(1,3-dichloro-2-propyl) phosphate (TDCPP) has received concerns due to its frequent detection in environmental media and biological samples. Our previous study has indicated TDCPP reduced the lifespan of Caenorhabditis elegans (C. elegans) by triggering an unconventional insulin/insulin-like growth factor signaling (IIS) pathway. This study continued to investigate the possible deleterious effects of TDCPP relating to longevity regulation signal pathways and biological processes. Specifically, this study uniquely performed small RNA transcriptome sequencing (RNA-seq), focusing on the underlying mechanisms of TDCPP-reduced the longevity of C. elegans in-depth in microRNAs (miRNAs). Based on Small RNA-seq results and transcript levels of mRNA involved in the unconventional IIS pathway, a small interaction network of miRNAs-mRNAs following TDCPP exposure in C. elegans was preliminarily established. Among them, up-regulated miR-48 and miR-84 (let-7 family members) silence the mRNA of daf-16 (the crucial member of the FoxO family and pivotal regulator in longevity) via post-transcription and translation dampening abilities, further inhibit its downstream target metallothionein-1 (mtl-1), and ultimately contributed to the reduction of nematode longevity and locomotion behaviors. Meanwhile, the high binding affinities of TDCPP with miRNAs cel-miR-48–5p and cel-miR-84–5p strongly support their participation in the regulation of nematode mobility and longevity. These findings provide a comprehensive analysis of TDCPP-reduced longevity from the perspective of miRNAs.
    Keywords Caenorhabditis elegans ; locomotion ; longevity ; microRNA ; phosphates ; sequence analysis ; transcriptome
    Language English
    Dates of publication 2022-0305
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 1491302-1
    ISSN 1873-3336 ; 0304-3894
    ISSN (online) 1873-3336
    ISSN 0304-3894
    DOI 10.1016/j.jhazmat.2021.128043
    Database NAL-Catalogue (AGRICOLA)

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  7. Article ; Online: Tris(1,3-dichloro-2-propyl) phosphate reduces longevity through a specific microRNA-mediated DAF-16/FoxO in an unconventional insulin/insulin-like growth factor‑1 signaling pathway.

    Wang, Chen / Li, Yeyong / Zeng, Lingjun / Shi, Chongli / Peng, Yi / Li, Hui / Chen, Haibo / Yu, Jun / Zhang, Jin / Cheng, Biao / Pan, Ruolin / Wang, Xiaoli / Xiang, Minghui / Huang, Yuan / Liu, Yongdi

    Journal of hazardous materials

    2021  Volume 425, Page(s) 128043

    Abstract: Tris(1,3-dichloro-2-propyl) phosphate (TDCPP) has received concerns due to its frequent detection in environmental media and biological samples. Our previous study has indicated TDCPP reduced the lifespan of Caenorhabditis elegans (C. elegans) by ... ...

    Abstract Tris(1,3-dichloro-2-propyl) phosphate (TDCPP) has received concerns due to its frequent detection in environmental media and biological samples. Our previous study has indicated TDCPP reduced the lifespan of Caenorhabditis elegans (C. elegans) by triggering an unconventional insulin/insulin-like growth factor signaling (IIS) pathway. This study continued to investigate the possible deleterious effects of TDCPP relating to longevity regulation signal pathways and biological processes. Specifically, this study uniquely performed small RNA transcriptome sequencing (RNA-seq), focusing on the underlying mechanisms of TDCPP-reduced the longevity of C. elegans in-depth in microRNAs (miRNAs). Based on Small RNA-seq results and transcript levels of mRNA involved in the unconventional IIS pathway, a small interaction network of miRNAs-mRNAs following TDCPP exposure in C. elegans was preliminarily established. Among them, up-regulated miR-48 and miR-84 (let-7 family members) silence the mRNA of daf-16 (the crucial member of the FoxO family and pivotal regulator in longevity) via post-transcription and translation dampening abilities, further inhibit its downstream target metallothionein-1 (mtl-1), and ultimately contributed to the reduction of nematode longevity and locomotion behaviors. Meanwhile, the high binding affinities of TDCPP with miRNAs cel-miR-48-5p and cel-miR-84-5p strongly support their participation in the regulation of nematode mobility and longevity. These findings provide a comprehensive analysis of TDCPP-reduced longevity from the perspective of miRNAs.
    MeSH term(s) Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism ; Insulin ; Insulin-Like Growth Factor I ; Longevity ; MicroRNAs/genetics ; Phosphates ; Signal Transduction
    Chemical Substances Caenorhabditis elegans Proteins ; Forkhead Transcription Factors ; Insulin ; MicroRNAs ; Phosphates ; daf-16 protein, C elegans ; Insulin-Like Growth Factor I (67763-96-6)
    Language English
    Publishing date 2021-12-09
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1491302-1
    ISSN 1873-3336 ; 0304-3894
    ISSN (online) 1873-3336
    ISSN 0304-3894
    DOI 10.1016/j.jhazmat.2021.128043
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Book: Qin cai you zhi gao xiao zai pei

    Tang, Xuejun / Li, Yeyong / Liu, Chunchang

    (San nong gong cheng shu ku ; Shu cai gao chan zai pei ji shu cong shu)

    2000  

    Author's details Tang Xuejun, Li Yeyong, Liu Chunchang bian zhu
    Series title San nong gong cheng shu ku
    Shu cai gao chan zai pei ji shu cong shu
    Keywords Celery.
    Language Chinese
    Size 69 p. :, ill. ;, 21 cm.
    Edition Di 1 ban.
    Publisher Giangxi ke xue ji xhu chu ban she ; Guangxi xin hua shu dian fa xing
    Publishing place Nanning shi
    Document type Book
    ISBN 7806199934 ; 9787806199930
    Database NAL-Catalogue (AGRICOLA)

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