DNA damage in HT‐29 colon cancer cells is enhanced by high concentrations of the anthocyanin malvidin

Non‐nutritive phytochemicals such as anthocyanins may reduce risk of chronic disease in part via antioxidant activity. However it is possible that at higher concentrations they may act as prooxidants and thus stimulate oxidative stress and apoptosis. The goal of our study was to determine whether the aglycone anthocyanins malvidin and peonidin act as antioxidants or prooxidants in vitro, with varying doses and cell types. HT‐29 human adenocarcinoma cells were plated in 12 well plates and incubated with 10, 25, or 50 μ mol/L malvidin or peonidin for two hours at 37°C, 95% CO 2 , 5% air. Cells were then incubated with 75 μ mol/L H 2 O 2 for 5 minutes. The Comet Assay (Trevigen) was performed to determine DNA damage, and apoptosis was assessed using a DNA fragmentation Cell Death Detection ELISA Plus kit (Roche). Neither malvidin nor peonidin decreased H 2 O 2 ‐induced DNA damage, and malvidin, but not peonidin, at 50 μ mol/L significantly increased (p<.05) H 2 O 2 induced DNA damage (control (8.5 ± 2.7); H 2 O 2 alone (13.7 ± 2.4); Malvidin 50 μ mol/L, (20.4 ± 3.3)). Data thus far suggests that even at concentrations of 10–50 μ mol/L malvidin and peonidin did not function as antioxidants to decrease H 2 O 2 induced DNA damage, and malvidin at 50 μ mol/L increased H 2 O 2 ‐induced DNA damage in HT‐29 cells. Support: GA Ag Exp Sta.