Neurotoxicity of halogenated organic compounds /

Detalles Bibliográficos
Clasificación:Libro Electrónico
Formato: eBook
Idioma:Inglés
Publicado: [S.l.] : Academic Press, 2023.
Colección:Advances in neurotoxicology ; 10
Temas:
Organohalogen compounds > Toxicology.
Neurotoxicology.
Compos�es organohalog�en�es > Toxicologie.
Neurotoxicologie.
Acceso en línea:Texto completo
Tabla de Contenidos:
  • Front Cover
  • Advances in Neurotoxicology
  • Copyright
  • Contents
  • Contributors
  • Preface
  • Chapter One: Perspective on halogenated organic compounds
  • 1 Introduction
  • 2 Background and classes of HOCs
  • 2.1 Chlorinated HOCs
  • 2.1.1 Physicochemical properties
  • 2.1.2 Environmental contamination and exposure to humans
  • 2.1.3 Effects on human health
  • 2.2 Brominated HOCs
  • 2.2.1 Physicochemical properties
  • 2.2.2 Environmental contamination and human exposure
  • 2.2.3 Effects on human health
  • 2.3 Fluorinated HOCs
  • 2.3.1 Physicochemical properties
  • 2.3.2 Environmental contamination and human exposure
  • 2.3.3 Effects on human health
  • 3 Summary and conclusions
  • Acknowledgments
  • References
  • Further reading
  • Chapter Two: The neurotoxicity of polychlorinated biphenyls (PCBs)
  • 1 Introduction
  • 2 Human studies
  • 2.1 Developmental neurotoxicity
  • 2.1.1 Yu-Cheng studies
  • 2.1.2 Michigan cohorts
  • 2.1.3 Dutch cohort
  • 2.1.4 German studies
  • 2.1.5 Faroe Islands cohort
  • 2.1.6 Oswego, New York cohort
  • 2.1.7 The New Bedford, Massachusetts studies
  • 2.1.8 Inuit cohort
  • 2.1.9 Flemish environmental health survey
  • 2.1.10 Rhea study, Crete, Greece
  • 2.1.11 Norwegian study
  • 2.1.12 The Collaborative Perinatal Project
  • 2.2 PCBs as environmental risk factors for neurodevelopmental disorders (NDDs)
  • 2.3 Data gaps in the human literature on PCB developmental neurotoxicity
  • 2.4 Neurotoxic outcomes in adults
  • 2.5 PCB effects on neurodegenerative diseases
  • 3 Experimental animal studies
  • 3.1 Learning and memory
  • 3.2 Motor function
  • 3.3 Attention
  • 3.4 Social behavior
  • 3.5 Insights from behavioral studies of mechanisms of PCB neurotoxicity
  • 4 Conclusions
  • Acknowledgments
  • Declaration of competing interests
  • References
  • Chapter Three: Neuroendocrine effects of polychlorinated biphenyls (PCBs).
  • 1 Introduction
  • 2 Overview of the hypothalamic-pituitary-gonadal and hypothalamic-pituitary-thyroid neuroendocrine systems
  • 2.1 Hormones and hypothalamic development
  • 2.2 Hypothalamic organization and differentiation
  • 2.3 Hormone receptors and differentiation
  • 2.4 The developmental origins of health and disease (DOHaD) hypothesis, and environmental epigenetics
  • 2.5 Epigenetic programming
  • 3 PCBs as environmental neuroendocrine disruptors
  • 4 PCBs effects on the hypothalamic-pituitary-gonadal axis
  • 4.1 Developmental exposures to PCBs: Effects on neuroendocrine systems
  • 4.2 Behavioral effects of developmental PCB exposures
  • 4.3 PCB effects on social behaviors
  • 4.4 PCB effects on reproductive and sociosexual behaviors
  • 4.5 PCB effects on anxiety and stress behaviors
  • 4.6 Molecular and cellular effects of developmental PCB exposure on the hypothalamus
  • 4.7 Human exposures to PCBs and neuroendocrine-related behaviors
  • 5 PCBs and the hypothalamic-pituitary-thyroid axis
  • 5.1 Background information on the thyroid system
  • 5.1.1 Role of deiodinases and cellular transporters
  • 5.1.2 The current model of the thyroid hormone system
  • 5.2 Evidence that PCBs affect brain development by interfering with the thyroid hormone system
  • 5.3 The effect of PCB exposures on human neurodevelopment
  • 6 Neuroendocrine effects of PCBs on the hypothalamo-neurohypophysial system (HNS)
  • 6.1 Organization of the HNS and its osmoregulatory function
  • 6.2 PCB effects on the peripheral vasopressin system
  • 6.2.1 PCB Effects on Vasopressin-Mediated Physiological Functions
  • 6.2.1.1 Role of nitric oxide (NO)
  • 6.3 PCB effects on the central vasopressin and oxytocin systems
  • 7 Inter- and transgenerational effects of PCBs on neuroendocrine systems
  • 7.1 Multigenerational A1221 effects: Neuroendocrine physiology and gene expression.
  • 7.2 Multigenerational PCB effects on behavior
  • 7.2.1 Epigenetic mechanisms of PCBs
  • 8 The future of toxicity testing for endocrine disruption: The ATHENA project on thyroid hormone system disruptors
  • Acknowledgments
  • References
  • Chapter Four: Ryanodine receptor-dependent mechanisms of PCB developmental neurotoxicity
  • 1 Introduction
  • 2 PCB-RyR interactions
  • 2.1 RyR structure and function
  • 2.2 PCB sensitization of the RyR
  • 3 RyR-dependent cellular effects of PCBs
  • 3.1 Dendritic arborization and synaptogenesis
  • 3.2 Neuronal apoptosis
  • 4 Evidence that RyR sensitization mediates the behavioral effects of PCBs
  • 4.1 Experimental animal studies
  • 4.2 Human studies
  • 5 Implications of RyR-dependent mechanisms of PCB developmental neurotoxicity
  • 5.1 RyR sensitization as a convergent mechanism of PCB developmental neurotoxicity
  • 5.2 Assessing PCB risks to the developing human brain
  • 5.3 Identifying gene-environment interactions that influence NDD risk
  • 6 Conclusions
  • Acknowledgments
  • Declaration of competing interests
  • References
  • Chapter Five: The microbiome/microbiota and the neurotoxicity of polybrominated diphenyl ether (PBDE) flame retardantsMicrobiome and PBDE neurotoxicity
  • 1 PBDEs: Uses, contamination, and body burden
  • 1.1 Uses
  • 1.2 Contamination
  • 1.3 Body burden
  • 2 Kinetics of PBDEs and structure-activity relationship considerations
  • 3 PBDEs: Adverse health effects
  • 4 Neurotoxicity of PBDEs
  • 5 Possible mechanisms of PBDE developmental neurotoxicity
  • 5.1 Effects of PBDEs on thyroid hormones
  • 5.2 PBDE-induced oxidative stress and consequent cell damage
  • 5.3 Other proposed mechanisms
  • 6 An overview of the microbiome and microbiota
  • 7 PBDEs and the microbiota
  • 7.1 Associations between PBDE exposure and fecal microbiota in humans.
  • 8 Effects of PBDEs on the microbiota and its association with neurotoxicity
  • 8.1 Evidence from human fecal microbiome
  • 8.2 Evidence from animal studies: Rodents
  • 8.3 Evidence from animal studies: Zebrafish
  • 9 Conclusions and future avenues for research
  • Acknowledgments
  • References
  • Chapter Six: Neuroendocrine effects of brominated flame retardants, focused on polybrominated diphenyl ethersNeuroendocrine effects of brominated flame retardants
  • 1 Introduction
  • 2 General characteristics of the main BFRs
  • 2.1 Polybrominated diphenyl ethers (PBDEs)
  • 2.2 Polybrominated biphenyls (PBBs)
  • 2.3 Hexabromocyclododecane (HBCD)
  • 2.4 Tetrabromobisphenol A (TBBPA)
  • 2.5 Novel brominated flame retardants (NBFRs)
  • 3 Overview of the neuroendocrine system
  • 4 Neuroendocrine disruption by BFRs
  • 5 Neuroendocrine effects of PBDEs
  • 5.1 PBDE effects on the HP-thyroid (HPT) axis
  • 5.1.1 In vitro studies
  • 5.1.2 Animal studies
  • 5.1.3 Human studies
  • 5.2 PBDE effects on the HP-gonadal (HPG) axis
  • 5.2.1 In vitro studies
  • 5.2.2 Animal studies
  • 5.2.3 Human studies
  • 5.3 PBDE effects on the HP-adrenal (HPA) axis
  • 5.4 PBDE effects on the HP-somatotropic (HPS) axis
  • 5.5 PBDE effects on the HN axis (oxytocin and arginine vasopressin)
  • 6 Neuroendocrine effects of PBBs
  • 6.1 PBB effects on the HPT axis
  • 6.2 PBB effects on the HPG axis
  • 6.3 PBB effects on the HPA axis
  • 7 Neuroendocrine effects of HBCD
  • 7.1 HBCD effects on the HPT axis
  • 7.2 HBCD effects on the HPG axis
  • 8 Neuroendocrine effects of TBBPA
  • 8.1 TBBPA effects on the HPT axis
  • 8.2 TBBPA effects on the HPG axis
  • 9 Neuroendocrine effects of NBFRs
  • 9.1 NBFR effects on the HPT axis
  • 9.2 NBFR effects on the HPG axis
  • 9.3 Metabolic disruption by NBFRs
  • 10 General conclusions
  • Acknowledgments
  • References.
  • Chapter Seven: Neurochemical effects of halogenated organic compounds: Possible adverse outcome pathways and structure-activity relationshipsNeurochemical effects of halogenated organic compounds
  • 1 Introduction
  • 2 Human (epidemiological studies) evidence of neurotoxicity by HOCs (PCBs and PBDEs)
  • 3 Evidence of neurotoxicity in animals by HOCs (PCBs and PBDEs)
  • 4 Neurotoxicity of HOCs (PCBs and PBDEs)-Potential adverse outcome pathways
  • 4.1 Perturbed calcium homeostasis and kinase signaling as a potential AOP for HOCs
  • 4.1.1 HOC effects on free calcium ([Ca2+]i) levels
  • 4.1.2 HOC effects on signal transduction pathways
  • 4.1.3 HOC effects on PKC isoforms in vivo
  • 4.1.4 HOC effects on genomic and proteomic changes in vivo
  • 4.1.5 HOC effects on structural and functional changes in vivo
  • 4.2 Perturbed thyroid hormone homeostasis as a potential AOP for HOCs
  • 4.3 Altered neurotransmitters and their function as a potential AOP for HOCs
  • 4.3.1 HOC effects on dopamine
  • 4.3.2 HOC effects on serotonin
  • 4.3.3 HOC effects on acetylcholine
  • 4.4 Oxidative stress as a potential AOP for HOCs
  • 5 Structure-activity relationships among HOCs (PCBs and PBDEs) on intracellular signaling events (PKC translocation and calcium buffering)
  • 5.1 SAR based on number of halogens with mixtures and congeners
  • 5.2 SAR based on position of halogens with HOC congeners
  • 5.3 SAR of structurally related HOCs: Role of planarity in the activity of HOCs
  • 5.4 SAR of structurally related HOCs: Similarities in the effects of PCBs and PBDEs
  • 5.5 Interactive effects of environmentally relevant HOCs (ex., PCBs, PCB metabolites, and dioxins)
  • 6 Summary and future directions
  • Acknowledgments
  • References
  • Chapter Eight: Neurotoxicity of poly- and perfluoroalkyl substances (PFAS): Epidemiological and rodent studies of behavioral outcomes.

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