Environmental contaminants and endocrine health /

Environmental Contaminants and Endocrine Health focuses specifically on contaminants with hormonal disrupting activities. The book provides insights into the multiple effects of endocrine-disrupting chemicals (EDCs) and their mechanism of action (MoA) on metabolism, reproduction and the multiple phy...

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Bibliographic Details
Corporate Author: ScienceDirect (Online service)
Other Authors: Carnevali, Oliana (Editor), Hardiman, Gary (Editor)
Format: eBook
Language:English
Published: London ; San Diego, CA : Academic Press, [2023]
Subjects:
Online Access:Connect to the full text of this electronic book
Table of Contents:
  • Intro
  • Environmental Contaminants and Endocrine Health
  • Copyright
  • Dedication
  • Contents
  • Contributors
  • Foreword
  • Preface
  • Acknowledgments
  • Chapter 1: Endocrine-disrupting chemical sources and effects
  • Chapter 1.1: Endocrine system
  • 1. Fundamentals of hormones
  • 1.1. Hormone classes
  • 1.1.1. Lipid-derived hormones
  • Steroid hormones
  • Eicosanoids
  • 1.1.2. Amino acid-derived hormones
  • 1.1.3. Peptide hormones
  • 1.2. Hormone receptors: Nuclear and membrane receptors
  • 1.2.1. The nuclear receptor superfamily
  • 1.2.2. Transmembrane receptors
  • 1.3. Hormone transport, peripheral metabolism, and clearance
  • 1.3.1. Hormone transport, binding proteins, and the role of the circulatory system
  • 1.3.2. Peripheral hormone metabolism and clearance
  • 2. Vertebrate endocrine physiology: Organs, axes, and hormones
  • 2.1. Hypothalamic-pituitary-gonadal (HPG) axis
  • 2.1.1. The hypothalamus and GnRH
  • 2.1.2. The anterior pituitary and gonadotropins
  • 2.1.3. The gonads, estrogens, androgens, and progestogens
  • 2.2. The adrenal glands and associated hormones and systems
  • 2.2.1. Overview of adrenal hormones
  • Corticosteroids: Glucocorticoids and mineralocorticoids
  • Catecholamines
  • Adrenal androgens
  • 2.2.2. Adrenal gland morphology
  • 2.2.3. Regulation of adrenal hormone secretion
  • The hypothalamic-pituitary-adrenal (HPA) axis
  • The renin-angiotensin-aldosterone system (RAAS)
  • 2.3. The hypothalamic-pituitary-thyroid (HPT) axis
  • 2.3.1. The hypothalamus and thyrotropin-releasing hormone (TRH)
  • 2.3.2. Anterior pituitary gland and thyrotropin (TSH)
  • 2.3.3. Thyroid gland and thyroid hormones
  • 2.4. The somatotropic axis
  • 2.5. Metabolic and nutritional endocrinology
  • 2.5.1. Hormonal control of feeding and digestion
  • 2.5.2. Hormonal control of nutrient and energy balance
  • 2.5.3. Adipose tissue endocrinology.
  • 2.5.4. Peroxisome proliferator-activated receptors
  • 2.6. Other vertebrate hormones and glands
  • References
  • Further reading
  • Chapter 1.2: Endocrine-disrupting chemicals (EDCs) in environmental matrices and human bodily fluids
  • 1. Introduction
  • 2. Endocrine-disrupting chemicals (EDCs)
  • 3. EDCs sources, exposure and presence in tissues and body fluids
  • 4. Plastics
  • 4.1. Plastics as EDCs
  • 4.2. Emerging chemical alternatives and the constantly changing landscape
  • 5. Pesticides
  • 6. Flame retardants
  • 7. Poly- and perfluoroalkyl substances (PFASs)
  • 8. Polychlorinated biphenyls (PCBs)
  • 9. Sunscreen
  • 10. Conclusion
  • References
  • Chapter 1.3: In vitro-, ecological-, murine, and human models for examining the effects of EDCs
  • 1. Summary
  • 2. In vitro models for examining the effects of EDCs
  • 3. Ecological models for examining the effects of EDCs
  • 4. Murine models for examining the effects of EDCs
  • 5. Human models for examining the effects of EDCs
  • 6. Overview
  • References
  • Chapter 1.4: Endocrine-disrupting chemicals and their mode of action: The case of nuclear receptors and the evolution of ...
  • 1. Introduction
  • 2. Evolution and nuclear receptors: A conceptual framework
  • 3. Endocrine disruption via nuclear receptors
  • 4. Conclusions
  • References
  • Chapter 1.5: EDCs impacts on human populations. Addressing multiple chemicals in human exposure and epidemiological studies
  • 1. Background
  • 1.1. How are we exposed?
  • 1.2. What is a mixture?
  • 1.3. How do we assess exposure to mixtures?
  • 1.4. What is biomonitoring?
  • 1.5. What are resulting data?
  • 1.6. How are exposure mixtures linked to health?
  • 2. Assessing chemical mixtures in a birth cohort study: A simulated example
  • 2.1. Simulation data
  • 2.2. Exposure continuum mapping (ECM)
  • 2.3. Stage 1: Exposure characterization with ECM.
  • 2.4. Estimation of joint health effects
  • 2.5. Results
  • 3. Conclusions
  • References
  • Chapter 2: Endocrine-disrupting chemicals as source of disease and health impairment in laboratory models
  • Chapter 2.1: EDCs: Focus on metabolic alteration of mammalian and nonmammalian models
  • 1. Introduction
  • 2. Approaches used to investigate the adverse actions of EDCs on the liver function
  • 2.1. Histological and histopathological evaluation of liver injury
  • 2.2. Glycogen storage assessment through histological staining
  • 2.3. Immunohistochemistry investigation of liver biomarkers
  • 2.4. Apoptosis
  • 2.5. Fourier-transform infrared spectroscopy hepatic characterization
  • 2.6. Targeted or total mRNA transcriptomics analysis
  • 2.7. RT-qPCR assessment of liver transcripts levels
  • 2.8. Quantification of protein levels by Western blot
  • 2.9. Hepatic proteomics analysis
  • 2.10. Metabolomics approach to study EDCs-induced liver alterations
  • 3. Hepatic metabolism alteration in nonmammalian model species: A 5-year survey
  • 3.1. Teleost liver metabolism alterations
  • 3.1.1. Bisphenols exposure
  • Bisphenol A
  • Bisphenols other than BPA
  • 3.1.2. Phthalates exposure
  • 3.1.3. Perfluoroalkylated substances (PFAs) exposure
  • 3.1.4. Glyphosate exposure
  • 3.2. Metabolic alterations in amphibians
  • 3.2.1. Plasticizer exposure
  • 3.2.2. PFOA exposure
  • 3.2.3. Glyphosate exposure
  • 4. Hepatic metabolism alteration in mammalian species: A 5-year survey
  • 4.1. Bisphenols exposure
  • 4.2. Phthalates exposure
  • 4.3. Perfluoroalkylated substances (PFAs) exposure
  • 4.4. Glyphosate exposure
  • 5. Conclusions
  • References
  • Chapter 2.2: EDCs: Focus on reproductive alterations in mammalian and nonmammalian models
  • 1. Introduction
  • 2. Reproductive toxicity outcomes in nonmammalian and mammalian species: A 5-year survey.
  • 2.1. Reproductive toxicity in teleost
  • 2.1.1. Exposure to BPA
  • Outcomes on male reproduction
  • Outcomes in female reproduction
  • 2.1.2. Exposure to bisphenol analogs other than BPA
  • Outcomes in male reproduction
  • Outcomes in female reproduction
  • 2.1.3. Exposure to phthalates
  • Outcomes in male reproduction
  • Outcomes in female reproduction
  • 2.1.4. Exposure to perfluoroalkylated substances (PFASs)
  • 2.2. Reproductive toxicity in amphibian models
  • 2.2.1. Toxicity of pesticides and herbicides
  • 2.2.2. Toxicity of phthalates and analogs
  • 2.3. Reproductive toxicity in mammalian models
  • 2.3.1. BPA, a recognized threat to reproduction in mammals
  • Outcomes in male reproduction
  • Outcomes in female reproduction
  • 2.3.2. Exposure to BPA alternatives: An emerging threat to mammalian reproduction
  • 2.3.3. Phthalates, recognized threats for mammalian reproduction
  • Outcomes in male reproduction
  • Outcomes in female reproduction
  • 2.3.4. PFASs, emerging threat for reproduction in mammals
  • Outcomes in male reproduction
  • Outcomes in female reproduction
  • 3. Are microplastics deleterious for reproduction in mammals?
  • 4. Conclusion
  • References
  • Chapter 2.3: The EDCs as epigenetic disruptors: Implications for development and health
  • 1. Introduction to epigenetics
  • 1.1. The epigenetic marks
  • 1.1.1. DNA methylation
  • 1.1.2. Histone modifications
  • 1.1.3. Noncoding RNAs
  • 1.2. Inheritance of epigenetic marks
  • 2. Interference of EDCs with the epigenetic dynamics
  • 3. The impact of epigenetic effects triggered by EDCs on health conditions
  • 3.1. Development and differentiation
  • 3.2. Metabolic disorders
  • 3.3. Reproductive disorders
  • 3.4. Neuroendocrine system and behavior
  • 3.5. Heart function and cardiovascular system
  • 4. Concluding remarks
  • References.
  • Chapter 2.4: Endocrine disrupting chemicals induce the epigenetic transgenerational inheritance of disease
  • 1. Introduction
  • 2. Molecular epigenetic mechanisms
  • 3. Epigenetic transgenerational inheritance
  • 4. Developmental etiology of epigenetic transgenerational inheritance
  • 5. Germline epimutations
  • 6. Transgenerational gene expression changes
  • 7. Conclusion
  • Acknowledgments
  • References
  • Chapter 2.5: Endocrine disruption persistence through development and across generations can be mediated by environmental ...
  • 1. Introduction
  • 2. Environmental perturbation of genome organization as DIPE mediator
  • 3. How do HEC perturbations determine the phenotypic manifestations of DIPE?
  • 4. How are HEC perturbations propagated?
  • 5. How are HEC perturbations originated?
  • 5.1. Preconception exposure and gamete perturbations
  • 5.2. Preconception exposure and F1 HEC perturbation
  • 5.3. Preconception exposure and F1 endocrine disruption putatively driven by HEC perturbations
  • 6. Concluding remarks
  • References
  • Chapter 2.6: Alterations of the endocannabinoid system by endocrine-disrupting chemicals: Effects on metabolism and repro ...
  • 1. The endocannabinoid system
  • 1.1. Endocannabinoids
  • 1.2. Endocannabinoid receptors
  • 1.3. Enzymatic machinery
  • 1.3.1. Anabolic enzymes
  • 1.3.2. Catabolic enzymes
  • 2. Endocannabinoid system, endocrine-disrupting chemicals, and hepatic metabolism
  • 2.1. Hepatic endocannabinoid system
  • 2.2. Endocrine-disrupting chemicals and hepatic endocannabinoid system
  • 2.2.1. Plastic polymers and plasticizers
  • 2.2.2. Polybrominated compounds
  • 2.2.3. Pesticides
  • 2.2.4. Parabens
  • 3. Endocannabinoid system, endocrine-disrupting chemicals, and reproduction
  • 3.1. Gonadal endocannabinoid system
  • 3.2. Endocrine-disrupting chemicals and gonadal endocannabinoid system
  • 3.2.1. Surfactants.