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• W2144198853 abstract "Gallic acid (GA) has various biological properties including anti-cancer effect. However, little is known about the toxicological effect of GA in primary normal cells. Here, we evaluated the effects of GA on human pulmonary fibroblast (HPF) cells in relation to reactive oxygen species (ROS) and glutathione (GSH). GA inhibited the growth of HPF cells at 24 hours in a dose-dependent manner. GA also induced HPF cell death, which was accompanied by the loss of mitochondrial membrane potential (MMP; ΔΨ m ). GA increased ROS levels including O 2 •- and GSH-depleted cell numbers in HPF cells at 24 hours. Treatment with 2 mM N-acetyl-cysteine (NAC) intensified growth inhibition and death in GA-treated HPF cells. NAC decreased ROS levels and increased GSH depletion in these cells. Treatment with 10 μM L-buthionine sulfoximine (BSO) also enhanced growth inhibition and death in GA-treated HPF cells. BSO increased ROS levels and GSH depletion in these cells. In conclusion, GA-induced HPF cell death was accompanied by ROS increase and GSH depletion. The changes of ROS and GSH levels by NAC and BSO appeared to affect cell growth and death in GA-treated HPF cells." @default.
• W2144198853 created "2016-06-24" @default.
• W2144198853 creator A5068413798 @default.
• W2144198853 creator A5079501124 @default.
• W2144198853 date "2010-10-04" @default.
• W2144198853 modified "2023-09-23" @default.
• W2144198853 title "Enhancement of gallic acid-induced human pulmonary fibroblast cell death by N-acetyl cysteine and L-buthionine sulfoximine" @default.
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• W2144198853 doi "https://doi.org/10.1177/0960327110384528" @default.
• W2144198853 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20921063" @default.
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