The role of the mitochondrial oxidative stress in the cytotoxic effects of the green tea catechin, (–)‐epigallocatechin‐3‐gallate, in oral cells. Issue 4 (18th November 2013)

• Record Type: Journal Article
• Authors: Tao, Ling; Forester, Sarah C.; Lambert, Joshua D.
• Is Part Of: Molecular nutrition & food research. Volume 58:Issue 4(2014:Apr.)
• Page Start: 665
• Page End: 676
• Publication Date: 2013-11-18
• Subjects: Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201300427
• Languages: English
• ISSNs: 1613-4125

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mnfr2108-sec-0010" sec-type="section"> <title>Scope</title> <p>The tea catechin, (–)‐epigallocatechin‐3‐gallate (EGCG), has potential cancer preventive effects. The prooxidant activity of EGCG may play a role in these effects.</p> </sec> <sec id="mnfr2108-sec-0020" sec-type="section"> <title>Methods and results</title> <p>Here, we report that EGCG exerted cytotoxic effects against oral cancer cell lines (IC<sub>50</sub> = 83–95 μM). EGCG treatment resulted in formation of extracellular reactive oxygen species (ROS), however, these ROS were rapidly cleared (half‐life = 1.7 h). EGCG treatment increased the production of mitochondrial H<sub>2</sub>O<sub>2</sub> in SCC‐25 cells (0–6 h) before the induction of apoptosis. Subsequently, an opening of the mitochondrial transition pore and a decrease in mitochondrial membrane potential were observed. The mitochondria‐specific antioxidant, MitoTEMPO, reduced these effects. HGF‐1 human gingival fibrobasts were resistant to EGCG (IC<sub>50</sub> > 200 μM) and EGCG‐induced ROS. EGCG induced differential expression of genes related to antioxidant defense in oral cancer cells and gingival fibroblasts: metallothionein 3, superoxide dismutase 2/3, and thioredoxin reductase 2 were downregulated in SCC‐25 cells, but upregulated in HGF‐1 cells.</p> </sec> <sec id="mnfr2108-sec-0030" sec-type="section"> <title>Conclusion</title> <p>We conclude that induction of mitochondrial ROS and mitochondrial dysfunction by EGCG play a role in the inhibition of oral cancer, and that gingival fibroblasts are spared from these effects in part because of a selective induction of antioxidant responsive genes.</p> </sec> </abstract>