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Antimony-induced alterations in thiol homeostasis and adenine nucleotide status in cultured cardiac myocytes.

Authors
Tirmenstein-MA; Mathias-PI; Snawder-JE; Wey-HE; Toraason-M
Source
Toxicology 1997 May; 119(3):203-211
NIOSHTIC No.
20033942
Abstract
Cultured cardiac myocytes were exposed for up to 4 h to 50 and 100 µM potassium antimonyl tartrate (PAT). After 4 h, 50 and 100 µM PAT killed 14 and 33% respectively of the cardiac myocytes. PAT-induced alterations in both protein and nonprotein thiol homeostasis. Transient increases in oxidized glutathione disulfide (GSSG) levels were detected after cells were treated with 100 µM PAT for 2 h. After 4 h, both concentrations of PAT significantly depleted reduced glutathione (GSH) levels. Protein thiols levels were also decreased after a 2-h exposure to 50 and 100 µM PAT. Cells treated with 50 µM and 100 µM PAT had a 15% and 40% reduction respectively in protein thiols after 4 h. PAT also significantly inhibited glutathione peroxidase and pyruvate dehydrogenase activity in cardiac myocytes. Pyruvate dehydrogenase activity levels were inhibited as early as 1 h after cells were treated with both concentrations of PAT. Cardiac myocyte ATP levels were also decreased by PAT, but only after a 4-h exposure to 50 µM and 100 µM PAT. Decreases in cellular ATP levels paralleled PAT toxicity put appeared to be secondary to other cellular changes initiated by PAT exposure.
Keywords
Antimony-compounds; Metal-compounds; Metallic-compounds; Heavy-metals; Cardiac-function; Thiols; Laboratory-animals; Animal-studies
CODEN
TXCYAC
CAS No.
70-18-8; 7440-36-0
Publication Date
19970516
Document Type
Journal Article
Fiscal Year
1997
Issue of Publication
3
ISSN
0300-483X
NIOSH Division
DBBS
Source Name
Toxicology
State
OH
Page last reviewed: April 12, 2019
Content source: National Institute for Occupational Safety and Health Education and Information Division