Cytoprotective effects of silymarin on epithelial cells against arsenic-induced apoptosis in contrast with quercetin cytotoxicity.

SORIA, ELIO A; EYNARD, ALDO R; BONGIOVANNI, GUILLERMINA A.

LIFE SCIENCES

PERGAMON-ELSEVIER SCIENCE LTD

Año: 2010 vol. 87 p. 309 - 315

0024-3205

The biomedical role of arsenic (As) is paradoxical, since it causes oxidative damage to normal cells leading to death or malignant transformation, and it can be used for the same reason as an anticancer pro-apoptotic agent at high doses, with substantial evidence indicating that alterations in control of oxidative stress and apoptosis contribute to As toxicity. Thus, the present study aimed to evaluate the potential effects of the flavonoids silymarin (S) and quercetin (Q) on arsenic-induced apoptosis in the non tumoral CHO-K1 cell line. Aqueous hydroperoxides (AHP), JNK (c-Jun N-terminal kinase) activation, caspase activity and death phenotype were assayed in order to establish the potential of S and Q as cancer chemopreventive and/or chemoadjuvant agents. Q probed to be toxic and did not exert complete protection against As, whereas only S was able to protect cells from the As-induced oxidative death, which started after 4 h with caspase activation and phosphatidylserine exteriorization on the outer cellular membrane. Although both flavonoids counteracted As-induced JNK activation (an early stress response, i.e exposure biomarker), AHP were increased by As and Q (p