Astrocytes as modulators of mercury-induced neurotoxicity

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

The case for significant toxicity of methylmercury (MeHg) to the CNS is strongly supported by both in vivo and in vitro studies. MeHg perturbs a number of cellular processes which most certainly include astrocytic failure to maintain the composition of the extracellular fluid. Astrocytic predisposition to be damaged by MeHg offers a potential explanation for its neurotoxicity. Consistent with this concept is the ability of astrocytes to preferentially concentrate brain MeHg. The present commentary elaborates on the role of astrocytes in mediating MeHg-induced injuries, detailing their function in maintaining the extracellular concentrations of the excitatory amino acids glutamate and aspartate. It continues with a discussion on the effects of MeHg on astrocytic swelling and the ensuing regulatory volume decrease (RVD). Recent work demonstrating that primary astrocyte cultures constituitively express a cluster of sulfhydryl (-SH)-containing proteins, collectively referred to as metallothioneins (MTs), is also reviewed with particular reference to the role of MTs both as protectors and facilitators of MeHg intoxication.

Original languageEnglish (US)
Pages (from-to)663-670
Number of pages8
JournalNeuroToxicology
Volume17
Issue number3-4
StatePublished - 1996
Externally publishedYes

Fingerprint

Mercury
Astrocytes
Modulators
Excitatory Amino Acids
Metallothionein
Extracellular Fluid
Aspartic Acid
Toxicity
Swelling
Glutamic Acid
Brain
Fluids
Wounds and Injuries
Chemical analysis
Proteins

Keywords

  • Astrocytes
  • Metallothionein
  • Methylmercury
  • Regulatory Volume Decrease (RVD)
  • Swelling

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Neuroscience(all)
  • Toxicology

Cite this

Astrocytes as modulators of mercury-induced neurotoxicity. / Aschner, Michael.

In: NeuroToxicology, Vol. 17, No. 3-4, 1996, p. 663-670.

Research output: Contribution to journalArticle

@article{e2ee3c6dfd2f4768823d5d941996d69c,
title = "Astrocytes as modulators of mercury-induced neurotoxicity",
abstract = "The case for significant toxicity of methylmercury (MeHg) to the CNS is strongly supported by both in vivo and in vitro studies. MeHg perturbs a number of cellular processes which most certainly include astrocytic failure to maintain the composition of the extracellular fluid. Astrocytic predisposition to be damaged by MeHg offers a potential explanation for its neurotoxicity. Consistent with this concept is the ability of astrocytes to preferentially concentrate brain MeHg. The present commentary elaborates on the role of astrocytes in mediating MeHg-induced injuries, detailing their function in maintaining the extracellular concentrations of the excitatory amino acids glutamate and aspartate. It continues with a discussion on the effects of MeHg on astrocytic swelling and the ensuing regulatory volume decrease (RVD). Recent work demonstrating that primary astrocyte cultures constituitively express a cluster of sulfhydryl (-SH)-containing proteins, collectively referred to as metallothioneins (MTs), is also reviewed with particular reference to the role of MTs both as protectors and facilitators of MeHg intoxication.",
keywords = "Astrocytes, Metallothionein, Methylmercury, Regulatory Volume Decrease (RVD), Swelling",
author = "Michael Aschner",
year = "1996",
language = "English (US)",
volume = "17",
pages = "663--670",
journal = "NeuroToxicology",
issn = "0161-813X",
publisher = "Elsevier",
number = "3-4",

}

TY - JOUR

T1 - Astrocytes as modulators of mercury-induced neurotoxicity

AU - Aschner, Michael

PY - 1996

Y1 - 1996

N2 - The case for significant toxicity of methylmercury (MeHg) to the CNS is strongly supported by both in vivo and in vitro studies. MeHg perturbs a number of cellular processes which most certainly include astrocytic failure to maintain the composition of the extracellular fluid. Astrocytic predisposition to be damaged by MeHg offers a potential explanation for its neurotoxicity. Consistent with this concept is the ability of astrocytes to preferentially concentrate brain MeHg. The present commentary elaborates on the role of astrocytes in mediating MeHg-induced injuries, detailing their function in maintaining the extracellular concentrations of the excitatory amino acids glutamate and aspartate. It continues with a discussion on the effects of MeHg on astrocytic swelling and the ensuing regulatory volume decrease (RVD). Recent work demonstrating that primary astrocyte cultures constituitively express a cluster of sulfhydryl (-SH)-containing proteins, collectively referred to as metallothioneins (MTs), is also reviewed with particular reference to the role of MTs both as protectors and facilitators of MeHg intoxication.

AB - The case for significant toxicity of methylmercury (MeHg) to the CNS is strongly supported by both in vivo and in vitro studies. MeHg perturbs a number of cellular processes which most certainly include astrocytic failure to maintain the composition of the extracellular fluid. Astrocytic predisposition to be damaged by MeHg offers a potential explanation for its neurotoxicity. Consistent with this concept is the ability of astrocytes to preferentially concentrate brain MeHg. The present commentary elaborates on the role of astrocytes in mediating MeHg-induced injuries, detailing their function in maintaining the extracellular concentrations of the excitatory amino acids glutamate and aspartate. It continues with a discussion on the effects of MeHg on astrocytic swelling and the ensuing regulatory volume decrease (RVD). Recent work demonstrating that primary astrocyte cultures constituitively express a cluster of sulfhydryl (-SH)-containing proteins, collectively referred to as metallothioneins (MTs), is also reviewed with particular reference to the role of MTs both as protectors and facilitators of MeHg intoxication.

KW - Astrocytes

KW - Metallothionein

KW - Methylmercury

KW - Regulatory Volume Decrease (RVD)

KW - Swelling

UR - http://www.scopus.com/inward/record.url?scp=0030425982&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030425982&partnerID=8YFLogxK

M3 - Article

VL - 17

SP - 663

EP - 670

JO - NeuroToxicology

JF - NeuroToxicology

SN - 0161-813X

IS - 3-4

ER -