Redox state in mediating methylmercury neurotoxicity

Marcelo Farina, Michael Aschner, João B.T. Rocha

Research output: Chapter in Book/Report/Conference proceedingChapter

5 Citations (Scopus)

Abstract

Methylmercury (MeHg) is an environmental pollutant that has been reported to induce neurotoxicity in both animals and humans. Although the molecular mechanisms underlying MeHg toxicity remain elusive, several lines of evidence indicate that MeHg is able to change the redox state of particular redox couples (i.e., reduced/oxidized glutathione (GSH), reduced/oxidized sulfhydryl or selenohydryl proteins, etc.), thus changing the entire cellular redox environment. These events contribute to oxidative stress, which culminates in neurotoxicity. Although MeHg-induced changes in the redox state are related to its direct interactions with nucleophilic molecules, such as GSH or sulfhydryl/selenohydryl proteins, it is noteworthy that MeHg can cause neurotoxicity even when present in concentrations 100- to 1,000fold less than those of these nucleophiles. Accordingly, recent evidence indicates that specific nucleophilic molecules (not yet fully identified) are primarily and/or preferentially targeted by MeHg due to their particular high reactivity toward this toxicant, thus initiating a cascade of molecular events that culminate in neurotoxicity. In this chapter, we give an initial background on the general concepts regarding the redox state and its important role in counteracting oxidative stress in the central nervous system, followed by discussions on the potential interaction of MeHg with redox couplers (mainly nucleophilic thiol- and selenol-containing molecules).

Original languageEnglish (US)
Title of host publicationMethylmercury and Neurotoxicity
PublisherSpringer US
Pages101-125
Number of pages25
ISBN (Electronic)9781461423836
ISBN (Print)9781461423829
DOIs
StatePublished - Jan 1 2012
Externally publishedYes

Fingerprint

Oxidation-Reduction
Oxidative Stress
Environmental Pollutants
Glutathione Disulfide
Sulfhydryl Compounds
Glutathione
Proteins
Central Nervous System

ASJC Scopus subject areas

  • Medicine(all)
  • Neuroscience(all)

Cite this

Farina, M., Aschner, M., & Rocha, J. B. T. (2012). Redox state in mediating methylmercury neurotoxicity. In Methylmercury and Neurotoxicity (pp. 101-125). Springer US. https://doi.org/10.1007/978-1-4614-2383-6_6

Redox state in mediating methylmercury neurotoxicity. / Farina, Marcelo; Aschner, Michael; Rocha, João B.T.

Methylmercury and Neurotoxicity. Springer US, 2012. p. 101-125.

Research output: Chapter in Book/Report/Conference proceedingChapter

Farina, M, Aschner, M & Rocha, JBT 2012, Redox state in mediating methylmercury neurotoxicity. in Methylmercury and Neurotoxicity. Springer US, pp. 101-125. https://doi.org/10.1007/978-1-4614-2383-6_6
Farina M, Aschner M, Rocha JBT. Redox state in mediating methylmercury neurotoxicity. In Methylmercury and Neurotoxicity. Springer US. 2012. p. 101-125 https://doi.org/10.1007/978-1-4614-2383-6_6
Farina, Marcelo ; Aschner, Michael ; Rocha, João B.T. / Redox state in mediating methylmercury neurotoxicity. Methylmercury and Neurotoxicity. Springer US, 2012. pp. 101-125
@inbook{2d9fba445d9c4870bb8da207203d19ce,
title = "Redox state in mediating methylmercury neurotoxicity",
abstract = "Methylmercury (MeHg) is an environmental pollutant that has been reported to induce neurotoxicity in both animals and humans. Although the molecular mechanisms underlying MeHg toxicity remain elusive, several lines of evidence indicate that MeHg is able to change the redox state of particular redox couples (i.e., reduced/oxidized glutathione (GSH), reduced/oxidized sulfhydryl or selenohydryl proteins, etc.), thus changing the entire cellular redox environment. These events contribute to oxidative stress, which culminates in neurotoxicity. Although MeHg-induced changes in the redox state are related to its direct interactions with nucleophilic molecules, such as GSH or sulfhydryl/selenohydryl proteins, it is noteworthy that MeHg can cause neurotoxicity even when present in concentrations 100- to 1,000fold less than those of these nucleophiles. Accordingly, recent evidence indicates that specific nucleophilic molecules (not yet fully identified) are primarily and/or preferentially targeted by MeHg due to their particular high reactivity toward this toxicant, thus initiating a cascade of molecular events that culminate in neurotoxicity. In this chapter, we give an initial background on the general concepts regarding the redox state and its important role in counteracting oxidative stress in the central nervous system, followed by discussions on the potential interaction of MeHg with redox couplers (mainly nucleophilic thiol- and selenol-containing molecules).",
author = "Marcelo Farina and Michael Aschner and Rocha, {Jo{\~a}o B.T.}",
year = "2012",
month = "1",
day = "1",
doi = "10.1007/978-1-4614-2383-6_6",
language = "English (US)",
isbn = "9781461423829",
pages = "101--125",
booktitle = "Methylmercury and Neurotoxicity",
publisher = "Springer US",

}

TY - CHAP

T1 - Redox state in mediating methylmercury neurotoxicity

AU - Farina, Marcelo

AU - Aschner, Michael

AU - Rocha, João B.T.

PY - 2012/1/1

Y1 - 2012/1/1

N2 - Methylmercury (MeHg) is an environmental pollutant that has been reported to induce neurotoxicity in both animals and humans. Although the molecular mechanisms underlying MeHg toxicity remain elusive, several lines of evidence indicate that MeHg is able to change the redox state of particular redox couples (i.e., reduced/oxidized glutathione (GSH), reduced/oxidized sulfhydryl or selenohydryl proteins, etc.), thus changing the entire cellular redox environment. These events contribute to oxidative stress, which culminates in neurotoxicity. Although MeHg-induced changes in the redox state are related to its direct interactions with nucleophilic molecules, such as GSH or sulfhydryl/selenohydryl proteins, it is noteworthy that MeHg can cause neurotoxicity even when present in concentrations 100- to 1,000fold less than those of these nucleophiles. Accordingly, recent evidence indicates that specific nucleophilic molecules (not yet fully identified) are primarily and/or preferentially targeted by MeHg due to their particular high reactivity toward this toxicant, thus initiating a cascade of molecular events that culminate in neurotoxicity. In this chapter, we give an initial background on the general concepts regarding the redox state and its important role in counteracting oxidative stress in the central nervous system, followed by discussions on the potential interaction of MeHg with redox couplers (mainly nucleophilic thiol- and selenol-containing molecules).

AB - Methylmercury (MeHg) is an environmental pollutant that has been reported to induce neurotoxicity in both animals and humans. Although the molecular mechanisms underlying MeHg toxicity remain elusive, several lines of evidence indicate that MeHg is able to change the redox state of particular redox couples (i.e., reduced/oxidized glutathione (GSH), reduced/oxidized sulfhydryl or selenohydryl proteins, etc.), thus changing the entire cellular redox environment. These events contribute to oxidative stress, which culminates in neurotoxicity. Although MeHg-induced changes in the redox state are related to its direct interactions with nucleophilic molecules, such as GSH or sulfhydryl/selenohydryl proteins, it is noteworthy that MeHg can cause neurotoxicity even when present in concentrations 100- to 1,000fold less than those of these nucleophiles. Accordingly, recent evidence indicates that specific nucleophilic molecules (not yet fully identified) are primarily and/or preferentially targeted by MeHg due to their particular high reactivity toward this toxicant, thus initiating a cascade of molecular events that culminate in neurotoxicity. In this chapter, we give an initial background on the general concepts regarding the redox state and its important role in counteracting oxidative stress in the central nervous system, followed by discussions on the potential interaction of MeHg with redox couplers (mainly nucleophilic thiol- and selenol-containing molecules).

UR - http://www.scopus.com/inward/record.url?scp=85026569895&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85026569895&partnerID=8YFLogxK

U2 - 10.1007/978-1-4614-2383-6_6

DO - 10.1007/978-1-4614-2383-6_6

M3 - Chapter

AN - SCOPUS:85026569895

SN - 9781461423829

SP - 101

EP - 125

BT - Methylmercury and Neurotoxicity

PB - Springer US

ER -