Curcumin is extensively used as a spice and pigment and has anticarcinogenic effects that could be linked to its antioxidant properties. However, some studies suggest that this natural compound possesses both pro- and antioxidative effects. In this study, we found that curcumin induced DNA damage to both the mitochondrial and nuclear genomes in human hepatoma G2 cells. Using quantitative polymerase chain reaction and immunocytochemistry staining of 8-hydroxydeoxyguanosine, we demonstrated that curcumin induced dose-dependent damage in both the mitochondrial and nuclear genomes and that the mitochondrial damage was more extensive. Nuclear DNA fragments were also evident in comet assays. The mechanism underlies the elevated level of reactive oxygen species and lipid peroxidation generated by curcumin. The lack of DNA damage at low doses suggested that low levels of curcumin does not induce DNA damage and may play an antioxidant role in carcinogenesis. But at high doses, we found that curcumin imposed oxidative stress and damaged DNA. These data reinforce the hypothesis that curcumin plays a conflicting dual role in carcinogenesis. Also, the extensive mitochondrial DNA damage might be an initial event triggering curcumin-induced cell death.

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Acrylamide (AA), a proven rodent carcinogen, has recently been discovered in foods heated at high temperatures. This finding raises public health concerns. In our previous study, we found that AA caused DNA fragments and increase of reactive oxygen species (ROS) formation and induced genotoxicity and weak cytotoxicity in HepG2 cells. Presently, curcumin, a natural antioxidant compound present in turmeric was evaluated for its protective effects. The results showed that curcumin at the concentration of 2.5 microg/mL significantly reduced AA-induced ROS production, DNA fragments, micronuclei formation, and cytotoxicity in HepG2 cells. The effect of PEG-catalase on protecting against AA-induced cytotoxicity suggests that AA-induced cytotoxicity is directly dependent on hydrogen peroxide production. These data suggest that curcumin could attenuate the cytotoxicity and genotoxicity induced by AA in HepG2 cells. The protection is probably mediated by an antioxidant protective mechanism. Consumption of curcumin may be a plausible way to prevent AA-mediated genotoxicity.

Hydroxytyrosol (HT), isolated from extra-virgin olive oil, possesses a marked antioxidant activity and is a good radical scavenger. In this study, our aim was to examine the anti-inflammatory mechanism of HT through measuring the inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) expression, TNF-alpha formation, and nitric oxide (NO) release in lipopolysaccharide (LPS)-induced human monocytic (THP-1) cells. Results showed that HT remarkably suppressed the LPS (1 microg/ml) induction of NO release. It also significantly attenuated the LPS-induced transcription of TNF-alpha, iNOS, and COX-2 in a dose-dependent manner. Furthermore, it was also found that HT in a concentration-dependent manner inhibited the expression of iNOS and COX-2 in THP-1 cells treated with 1 microg/ml LPS using Western Blot. Taken together, these results suggest that HT exerts anti-inflammatory effects probably through the suppression of COX-2 and iNOS expression.

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