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Effects of rosmarinic acid against aflatoxin B 1 and ochratoxin‐A‐induced cell damage in a human hepatoma cell line (Hep G2)
Author(s) -
Renzulli C.,
Galvano F.,
Pierdomenico L.,
Speroni E.,
Guerra M. C.
Publication year - 2004
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.982
Subject(s) - rosmarinic acid , ochratoxin a , hep g2 , cell culture , cell , chemistry , mycotoxin , biochemistry , biology , food science , genetics , antioxidant
Recent ndings have suggested that oxidative damage might contribute to the cytotoxicity and carcinogenicity of aatoxin B 1 (AFB 1 ). The induction of oxidative stress also plays an important role in the toxicity of another mycotoxin: ochratoxin A (OTA). In this study, the protective effect of rosmarinic acid (Ros A) against AFB 1 and OTA‐induced cytotoxicity was investigated in a human hepatoma‐derived cell line (Hep G2). Rosmarinic acid, a natural phenolic compound contained in many Lamiaceae herbs such as Perilla frutescens , sage, basil and mint, inhibits complement‐dependent inammatory processes and may have therapeutic potential. The ability of Ros A to reduce radical oxygen species (ROS) production, protein and DNA synthesis inhibition and apoptosis caused by the two mycotoxins was also investigated. Our experiments proved the signicant cytoprotective effect of Ros A in vitro from OTA‐ and AFB 1 ‐induced cell damage. In particular, 24‐h pretreatment with 50 µM Ros A inhibited the cytotoxicity of 10 µM AFB 1 (by 45%) and 10 µM OTA (by 35%) in Hep G2 cells ( P < 0.001). Moreover, Ros A dose dependently attenuated ROS production and DNA and protein synthesis inhibition induced by both of the toxins. Similarly, apoptosis cell death was prevented, as demonstrated by reduction of DNA fragmentation and inhibition of caspase‐3 activation ( P < 0.001). Copyright © 2004 John Wiley & Sons, Ltd.