NDLI: Gallic acid induces HeLa cell death via increasing GSH depletion rather than ROS levels.

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Gallic acid induces HeLa cell death via increasing GSH depletion rather than ROS levels.

Content Provider	Semantic Scholar
Author	Park, Woo Hyun
Copyright Year	2017
Abstract	Gallic acid (GA; 3,4,5-triphydroxyl-benzoic acid) is widely dispersed in various plants, fruits and foods and it shows various biological properties including anticancer effects. This study investigated the effects of GA on HeLa cervical cancer cells in relation to cell death, reactive oxygen species (ROS) and glutathione (GSH). GA dose-dependently inhibited the growth of HeLa cells and human umbilical vein endothelial cells (HUVEC) at 24 or 72 h. The susceptibility of HeLa cells to GA was higher than that of HUVEC. GA induced apoptosis in HeLa cells, which was accompanied by the loss of mitochondrial membrane potential (MMP; ∆ψm). GA increased ROS levels including O2•- in HeLa cells at 24 h and it also induced GSH depletion. N-acetyl cysteine (NAC) increased the growth inhibition of GA-treated HeLa cells and enhanced the death of these cells. NAC differently influenced ROS levels in GA-treated HeLa cells and significantly increased GSH depletion in these cells. L-buthionine sulfoximine (BSO) increased MMP (∆ψm) loss, ROS levels and GSH depletion in GA-treated HeLa cells. In conclusion, GA significantly inhibited the growth of HeLa cells. GA-induced HeLa cell death was tightly related to GSH depletion rather than ROS level changes.
Starting Page	1277
Ending Page	1283
Page Count	7
File Format	PDF HTM / HTML
DOI	10.3892/or.2016.5335
PubMed reference number	28035417
Journal	Medline
Volume Number	37
Issue Number	2
Alternate Webpage(s)	https://www.spandidos-publications.com/or/37/2/1277/download
Alternate Webpage(s)	https://doi.org/10.3892/or.2016.5335
Journal	Oncology reports
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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