RT Journal Article SR Electronic T1 Autoxidation of Gallic Acid Induces ROS-dependent Death in Human Prostate Cancer LNCaP Cells JF Anticancer Research JO Anticancer Res FD International Institute of Anticancer Research SP 1595 OP 1602 VO 32 IS 5 A1 LARRY H. RUSSELL, JR A1 ELIZABETH MAZZIO A1 RAMESH B. BADISA A1 ZHI-PING ZHU A1 MARYAM AGHARAHIMI A1 EBENEZER T. ORIAKU A1 CARL B. GOODMAN YR 2012 UL http://ar.iiarjournals.org/content/32/5/1595.abstract AB Background: Prostate cancer is the second most common cause of mortality. Gallic acid (GA) is a natural polyphenol, and we tested its in-vitro cytotoxicity after 24 h in prostate cancer LNCaP cells. Materials and Methods: GA autoxidation was measured fluorimetrically for H2O2, and O2•− radicals by chemiluminescence. Intracellular reactive oxygen species (ROS) levels were detected with 2’,7’-dichlorodihydrofluorescein diacetate. Cytotoxicity was evaluated by crystal-violet, while apoptosis and mitochondrial membrane potential were determined by flow cytometry. Cytochrome c release was detected by enzyme-linked immunosorbent assay, and caspase-8, -9 and -3 activities were measured calorimetrically. Results: GA autoxidation produced significant levels of H2O2 and O2.-. Increased intracellular ROS levels with GA were reduced by N-acetyl-L-cysteine (NAC) and L-glutathione (GSH). Cells were protected against GA cytotoxicity when pretreated with increasing levels of superoxide dismutase/catalase mixture, NAC, or GSH for 3 h. The number of apoptotic cells increased with GA dose. GA caused mitochondrial potential loss, cytochrome c release, and activation of caspases 3, 8 and 9. Conclusion: The ROS-dependent apoptotic mechanism of GA kills malignant cells effectively; it is likely that GA could be a good anticancer agent.