Fetal minamata disease: A human episode of congenital methylmercury poisoning

Alessandra A. Dos Santos; Louis W. Chang; Grace Liejun Guo; Michael Aschner

doi:10.1016/B978-0-12-809405-1.00035-3

Fetal minamata disease: A human episode of congenital methylmercury poisoning

Alessandra A. Dos Santos, Louis W. Chang, Grace Liejun Guo, Michael Aschner

Molecular Pharmacology

Research output: Chapter in Book/Report/Conference proceeding › Chapter

17 Scopus citations

Abstract

This chapter addresses well-known episodes of methylmercury (MeHg) poisoning, highlighting differences between the epidemics in Minamata Bay, Japan, and Iraq. Special attention is directed to the cognitive effects of MeHg in neonates and children, and the underlying changes in cytoarchitecture. Finally, we discuss the biomolecular basis of neurotoxicity in fetal Minamata disease emphasizing neural cell adhesion molecule and changes in neuronal cytoskeletal proteins. Cell polarization and migration patterns require dynamic rearrangement of the actin and microtubule cytoskeletons via intracellular signaling pathways involving Rho family GTPases. The Rho-associated protein kinases are central regulators of the actin cytoskeleton downstream of the small GTPase Rho and their role is discussed within the context of MeHg-induced injury.

Original language	English (US)
Title of host publication	Handbook of Developmental Neurotoxicology
Publisher	Elsevier
Pages	399-406
Number of pages	8
ISBN (Electronic)	9780128094051
DOIs	https://doi.org/10.1016/B978-0-12-809405-1.00035-3
State	Published - Jan 1 2018

Keywords

Methylmercury
Microtubules
Minamata disease
Neurotoxicity
Rho-associated protein kinases (ROCKs)

ASJC Scopus subject areas

General Neuroscience

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/B978-0-12-809405-1.00035-3

Cite this

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title = "Fetal minamata disease: A human episode of congenital methylmercury poisoning",

abstract = "This chapter addresses well-known episodes of methylmercury (MeHg) poisoning, highlighting differences between the epidemics in Minamata Bay, Japan, and Iraq. Special attention is directed to the cognitive effects of MeHg in neonates and children, and the underlying changes in cytoarchitecture. Finally, we discuss the biomolecular basis of neurotoxicity in fetal Minamata disease emphasizing neural cell adhesion molecule and changes in neuronal cytoskeletal proteins. Cell polarization and migration patterns require dynamic rearrangement of the actin and microtubule cytoskeletons via intracellular signaling pathways involving Rho family GTPases. The Rho-associated protein kinases are central regulators of the actin cytoskeleton downstream of the small GTPase Rho and their role is discussed within the context of MeHg-induced injury.",

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AU - Chang, Louis W.

AU - Guo, Grace Liejun

AU - Aschner, Michael

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AB - This chapter addresses well-known episodes of methylmercury (MeHg) poisoning, highlighting differences between the epidemics in Minamata Bay, Japan, and Iraq. Special attention is directed to the cognitive effects of MeHg in neonates and children, and the underlying changes in cytoarchitecture. Finally, we discuss the biomolecular basis of neurotoxicity in fetal Minamata disease emphasizing neural cell adhesion molecule and changes in neuronal cytoskeletal proteins. Cell polarization and migration patterns require dynamic rearrangement of the actin and microtubule cytoskeletons via intracellular signaling pathways involving Rho family GTPases. The Rho-associated protein kinases are central regulators of the actin cytoskeleton downstream of the small GTPase Rho and their role is discussed within the context of MeHg-induced injury.

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KW - Microtubules

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KW - Neurotoxicity

KW - Rho-associated protein kinases (ROCKs)

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BT - Handbook of Developmental Neurotoxicology

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ER -

Fetal minamata disease: A human episode of congenital methylmercury poisoning

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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