Journal
EUROPEAN JOURNAL OF NUTRITION
Volume 54, Issue 2, Pages 223-234Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00394-014-0703-2
Keywords
Glutathione; Hyperglycemia; Liver; Reactive oxygen species; Injury
Categories
Funding
- Department of Biotechnology, New Delhi, India
- Veterans Administration
- Council of Scientific and Industrial Research (CSIR), New Delhi, India
- DBT
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The deficiency of glutathione (GSH) has been linked to several diseases. The study investigated the role of GSH as a protective factor against hyperglycemia-mediated injury in VL-17A cells treated with 50 mM glucose. The cell viability and different oxidative stress parameters including glyoxalase I activity were measured. GSH supplementation with 2 mM N-acetyl cysteine (NAC) or 0.1 mM ursodeoxycholic acid (UDCA) increased the viability, GSH level and the GSH-dependent glyoxalase I activity in 50 mM glucose-treated VL-17A cells. Further, pretreatment of 50 mM glucose-treated VL-17A cells with NAC or UDCA decreased oxidative stress (levels of reactive oxygen species and protein carbonylation), apoptosis (caspase 3 activity and annexin V-propidium iodide positive cells) and glutathionylated protein formation, a measure of oxidative stress. GSH depletion with 0.4 mM buthionine sulfoximine (BSO) or 1 mM diethyl maleate (DEM) potentiated the decrease in viability, glyoxalase I activity and increase in oxidative stress and apoptosis, with decreased GSH levels in 50 mM glucose-treated VL-17A cells. Thus, changes in GSH levels with exogenous agents such as NAC, UDCA, BSO or DEM modulate hyperglycemia-mediated injury in a cell model of VL-17A liver cells.
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