Autoxidation of Gallic Acid Induces ROS-dependent Death in Human Prostate Cancer LNCaP Cells

Overview

Journal Anticancer Res

Specialty Oncology

Date 2012 May 18

PMID 22593437

Citations 28

Authors

Larry H Russell Jr

Elizabeth Mazzio

Ramesh B Badisa

Zhi-Ping Zhu

Maryam Agharahimi

Ebenezer T Oriaku

Carl B Goodman

Affiliations

Soon will be listed here.

Abstract

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 H(2)O(2), and O(2)(•-) 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 H(2)O(2) 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.

Citing Articles

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