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Int J Mol Med. 2009 Aug;24(2):261-8.

The effects of buthionine sulfoximine, diethyldithiocarbamate or 3-amino-1,2,4-triazole on propyl gallate-treated HeLa cells in relation to cell growth, reactive oxygen species and glutathione.

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  • 1Department of Physiology, Medical School, Center for Healthcare Technology Development, Institute for Medical Sciences, Chonbuk National University, JeonJu 561-180, Korea.

Abstract

Propyl gallate (PG) as a synthetic antioxidant is widely used in processed food and medicinal preparations. It also exerts a variety of effects on tissue and cell functions. In the present study, we investigated the effects of L-buthionine sulfoximine (BSO, an inhibitor of GSH synthesis), diethyldithiocarbamate (DDC, an inhibitor of Cu/Zn-SOD) or 3-amino-1,2,4-triazole (AT, an inhibitor of catalase) on PG-treated HeLa cells in relation to cell growth, reactive oxygen species (ROS) and glutathione (GSH). Treatment with PG induced growth inhibition, the loss of mitochondrial membrane potential [MMP (DeltaPsim)] and apoptosis in HeLa cells. ROS levels including O2.- were increased or decreased in PG-treated HeLa cells depending on the incubation times. PG caused depletion in GSH content in HeLa cells. While BSO enhanced the growth inhibition of PG-treated HeLa cells at 4 h, DDC and AT did not. All the agents down-regulated MMP (DeltaPsim) levels in PG-treated cells. Although BSO, DDC or AT slightly increased ROS or O2.- levels in PG-treated cells at 1 h, these enhancements of ROS did not intensify apoptosis in these cells. In addition, BSO, DDC or AT slightly reduced GSH level in PG-treated HeLa cells at 1 h, but this reduction did not affect cell death of HeLa. Furthermore, PG induced a G1 phase arrest of the cell cycle. BSO, DDC or AT significantly inhibited the G1 phase arrest in PG-treated cells. Conclusively, the changes of ROS and GSH levels by BSO, DDC or AT in PG-treated HeLa cells did not strongly affect the cell growth and death.

PMID:
19578799
[PubMed - indexed for MEDLINE]
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