TY - JOUR T1 - Autoxidation of Gallic Acid Induces ROS-dependent Death in Human Prostate Cancer LNCaP Cells JF - Anticancer Research JO - Anticancer Res SP - 1595 LP - 1602 VL - 32 IS - 5 AU - LARRY H. RUSSELL, JR AU - ELIZABETH MAZZIO AU - RAMESH B. BADISA AU - ZHI-PING ZHU AU - MARYAM AGHARAHIMI AU - EBENEZER T. ORIAKU AU - CARL B. GOODMAN Y1 - 2012/05/01 UR - http://ar.iiarjournals.org/content/32/5/1595.abstract N2 - 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. ER -