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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| Format: | eBook |
| Language: | English |
| Published: |
London ; San Diego, CA :
Academic Press,
[2023]
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| 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.