Protection against ultraviolet B-induced oxidative DNA damage in rabbit corneal-derived cells (SIRC) by 4-coumaric acid

The exposure of cells to ultraviolet B radiation (UV-B) can induce the production of reactive oxygen species (ROS) which damage cellular components. Free radical scavengers and antioxidants can interfere with the production of ROS. We measured 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, a marker of oxidative DNA damage in rabbit cornealderived cells (SIRC) exposed to UV-13 in the presence of 4-coumaric acid, a natural polyphenol. The levels of 8-OHdG were increased significantly (P < 0.01) following irradiation (from 12 +/- 1.2 x 10(-6) to 29 +/- 6.2 x 10(-6) dG, means +/- SE). When 10 muM 4-coumaric acid was added to the medium, 8-OHdG levels were similar to those of unexposed cells (16.8 +/- 0.8 x 10(-6) dG). UV-B irradiation decreased superoxide dismutase (SOD) activity in SIRC cells from 0.29 +/- 0.6 to 0.15 +/- 0.04 mU/mg (means +/- SE). The presence of 10 muM 4-coumaric acid prevented the decrease in SOD activity (0.20 +/- 0.05 mU/mg, P < 0.05). On the contrary, SIRC cells exposed to UV-B had higher levels of xanthine oxidase (XO) activity compared with control ones (0.40 +/- 0.07 and 0.24 +/- 0.08 mU/mg, means +/- SE, respectively). In the presence of 10 muM 4-coumaric acid, the increase in XO activity was prevented (0.16 +/- 0.03 mU/mg; mean +/- SE). In conclusion, UV-B-induced oxidative DNA damage in SIRC cells is inhibited by 4-coumaric acid, which, probably through its free radical scavenging activity, stabilizes SOD activity and blocks the increase of XO activity following UV-B irradiation. Thus, the topical use of 4-coumaric acid may prevent free radical damage in the cornea. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.