Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-12-17
pubmed:abstractText
Maintenance of appropriate intracellular glutathione (GSH) levels is crucial for cellular defense against oxidative damage. A suggested mechanism of methylmercury (MeHg) neurotoxicity implicates the involvement of oxygen radical formation and a decrease in cellular levels of GSH. Astrocytes play an important role in providing GSH precursors to neurons, and as will be discussed in this review, altered GSH homeostasis likely leads to impairment of astrocytic handling of glutamate, and neuronal energy metabolism. The review summarizes recent observations on transport systems for cysteine and cystine, precursors of GSH, in primary cultures of astrocytes and neurons, and their sensitivity to MeHg treatment.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0360-4012
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
66
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
998-1002
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Identification and characterization of uptake systems for cystine and cysteine in cultured astrocytes and neurons: evidence for methylmercury-targeted disruption of astrocyte transport.
pubmed:affiliation
Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1083, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review