Linked Life Data

15261164

Source:http://linkedlifedata.com/resource/pubmed/id/15261164

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2004-7-20
pubmed:abstractText
The molecular basis of the toxic properties of phenoxy herbicides in humans and animals has been insufficiently studied. In this study, damage parameters [levels of reduced glutathione (GSH) and total glutathione; activity of glutathione reductase (GR); activities of catalase (CAT) and superoxide dismutase (SOD); levels of adenine nucleotides and adenine energy charge (AEC)] were measured in human erythrocytes exposed in vitro to 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) and its metabolite 2,4,5-trichlorophenol (2,4,5-TCP). Both 2,4,5-T and 2,4,5-TCP decreased the level of reduced glutathione (GSH) in erythrocytes in comparison to the control, but did not significantly change the total glutathione (2GSH + GSSG). This suggests that GSH concentration decreases concomitantly with an increase in oxidized glutathione (GSSG). 2,4,5-TCP at 100 ppm significantly decreased catalase and SOD activities. 2,4,5-T and 2,4,5-TCP did not significantly change the activity of glutathione reductase. 2,4,5-TCP decreased the level of ATP and increased the content of ADP and AMP, indicating a fall in AEC. 2,4,5-T and 2,4,5-TCP significantly changed the erythrocyte morphology. All these data are evidence of oxidative stress in erythrocytes incubated with 2,4,5-T and 2,4,5-TCP; the stress appears to be more intense in the case of 2,4,5-TCP.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1065-6995
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
557-63
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
2,4,5-T and 2,4,5-TCP induce oxidative damage in human erythrocytes: the role of glutathione.
pubmed:affiliation
Department of Biophysics of Environmental Pollution, University of Lodz, Banacha 12/16, 90-237 Lodz, Poland. bukow@biol.uni.lodz.pl
pubmed:publicationType
Journal Article