期刊
JOURNAL OF BERRY RESEARCH
卷 6, 期 2, 页码 125-136出版社
IOS PRESS
DOI: 10.3233/JBR-160122
关键词
Cranberry proanthocyanidins; esophageal adenocarcinoma; Barrett's esophagus; ROS; JHAD1; OE33; OE19; CP-C; hydrogen peroxide
资金
- National Institutes of Health
- National Cancer Institute [RO1-CA158319]
- Advancing a Healthier Wisconsin [5220296]
BACKGROUND: We recently reported that a cranberry proanthocyanidin rich extract (C-PAC) induces autophagic cell death in apoptotic resistant esophageal adenocarcinoma (EAC) cells and necrosis in autophagy resistant cells. EAC is characterized by high morbidity and mortality rates supporting development of improved preventive interventions. OBJECTIVE: The current investigation sought to investigate the role of reactive oxygen species (ROS) in the context of C-PAC induced cell death. METHODS: Apanel of human esophageal cell lines of EAC or BE (Barrett's esophagus) origin were treated with C-PAC and assessed for ROS modulation using CellROX (R) Green reagent and the Amplex Red assay to specifically measure hydrogen peroxide levels. RESULTS: C-PAC significantly increased ROS levels in EAC cells, but significantly reduced ROS levels in CP-C BE cells. Increased hydrogen peroxide levels were also detected in C-PAC treated EAC cells and supernatant; however, hydrogen peroxide levels were significantly increased in medium alone, without cells, suggesting that C-PAC interferes or directly acts on the substrate. Hydrogen peroxide levels did not change in C-PAC treated CP-C BE cells. CONCLUSION: These experiments provide additional mechanistic insight regarding C-PAC induced cancer cell death through modulation of ROS. Additional research is warranted to identify specific ROS species associated with C-PAC exposure.
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