Abstract:
:Sodium diethyldithiocarbamate (DETC) is the main metabolite of disulfiram. Recently, we reported that mechanism of disulfiram cytotoxicity in V79 cells might be partially connected with thiol redox-state imbalance. Here, we examined the effect of DETC on the level of intracellular glutathione (GSH), protein oxidation (measured as PC-protein carbonyl content), lipid peroxidation (measured as TBARS-thiobarbituric acid reactive substances), antioxidant enzymatic defense, as well as on apoptosis. We used V79 Chinese hamster fibroblasts cells with and without modulated glutathione (GSH) level by N-acetyl-L-cysteine (NAC). We showed that treatment with DETC at concentrations that cause a moderate increase in thiol-state imbalance but not cell death stimulates oxidative stress measured as increased level of PC and TBARS, adaptive response of GSH-related enzymes and apoptosis. Our results show that cellular effects of DETC are partially attributable to the initial redox cellular state, since the increase of GSH level by NAC pre-treatment prevented the observed changes.
journal_name
Arch Toxicoljournal_title
Archives of toxicologyauthors
Rahden-Staroń I,Grosicka-Maciąg E,Kurpios-Piec D,Czeczot H,Grzela T,Szumiło Mdoi
10.1007/s00204-012-0909-0subject
Has Abstractpub_date
2012-12-01 00:00:00pages
1841-50issue
12eissn
0340-5761issn
1432-0738journal_volume
86pub_type
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