GSH protects against oxidative stress and toxicity in VL-17A cells exposed to high glucose

S. Mathan Kumar, Kavitha Swaminathan, Dahn L. Clemens, Aparajita Dey

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


Purpose: 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. Methods: The cell viability and different oxidative stress parameters including glyoxalase I activity were measured. Results: 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. Conclusion: 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.

Original languageEnglish (US)
Pages (from-to)223-234
Number of pages12
JournalEuropean Journal of Nutrition
Issue number2
StatePublished - Mar 2015


  • Glutathione
  • Hyperglycemia
  • Injury
  • Liver
  • Reactive oxygen species

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Nutrition and Dietetics


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