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Cytotoxic and proapoptotic activities of gallic acid to human oral cancer HSC-2 cells

Alyssa G. Schuck, Jeffrey H. Weisburg, Hannah Esan, Esther F. Robin, Ayelet R. Bersson, Jordana R. Weitschner, Tova Lahasky, Harriet L. Zuckerbraun, Harvey Babich.

Cited by (4)

Abstract
Human carcinoma HSC-2 cells were more sensitive to a 24 h exposure to gallic acid than were normal human gingival fibroblasts. Acting as a prooxidant, gallic acid generated hydrogen peroxide in cell culture medium. The potency of gallic acid to HSC-2 cells was significantly lessened in the presence of scavengers of hydrogen peroxide, including catalase, pyruvate, and divalent cobalt cations, and was potentiated in the presence of the intracellular glutathione depleters, 1-chloro-2,4-dinitrobenzene, bis(2-chloroethyl)-N-nitrosourea, and DL-buthionine-[S,R]-sulfoximine. Exposure of HSC-2 cells to gallic acid decreased the level of intracellular reduced glutathione, caused lipid peroxidation, and increased the level of intracellular reactive oxygen species. Flow cytometric analyses of gallic acid-treated HSC-2 cells indicated a concentration-dependent response for the induction of apoptosis, which was reversed in the presence of divalent cobalt. Immunoblot analyses of gallic acid-treated cells showed proteolytic inactivation of poly(ADP-ribose) polymerase, an indication of apoptosis, which was also reversed in the presence of divalent cobalt cations. These studies demonstrated that the cytotoxic activities of gallic acid to HSC-2 cells were mediated through autooxidation of the polyphenol, leading to the induction of oxidative stress and thereby apoptotic cell death.

Key words: Gallic acid; Nutraceuticals; Oral cancer; Oxidative stress; Polyphenols; Prooxidants



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