Evidence for a Role of Oxidative Stress in the Carcinogenicity of Ochratoxin A

Figure 1

Scheme to illustrate the oxidative stress-mediated mode of action proposed for OTA. Increased production of ROS, RNS, and RCS is likely to originate either from direct redox reactions involving OTA or through the inhibition of cellular defenses such as through the inhibition of transcription factors as Nrf2 which regulates enzymes with antioxidant properties. The generation of radicals will induce macromolecular oxidative damage such as oxidized DNA bases which may be converted into mutation resulting into generation of transformed cells. In addition, radicals will trigger biological responses which may impair intercellular communication and induce cell proliferation as well as reduction in cellular defense in oxidative stress. This last effect is likely to amplify the oxidative stress-mediated effects of OTA. Altogether, these molecular mechanisms will result in cancer development.