title: Lycopene enhances UVA-induced DNA damage and expression of heme oxygenase-1 in cultured mouse embryo fibroblasts.
abstract: BACKGROUND
  It has been suggested that carotenoids including lycopene may reduce the risk of photodamage. However, carotenoids are unstable under light exposure and may produce prooxidative effects under certain circumstances.
  
  
  OBJECTIVE
  We examined whether lycopene inhibits ultraviolet A (UVA)-induced DNA damage and the expression of heme oxygenase-1 (HO-1). We hypothesized that the breakdown of lycopene by UVA irradiation, rather than intact lycopene itself, causes oxidative damage.
  
  
  METHODS
  Mouse fibroblasts, C3H10T1/2 (C3H), were first enriched with 10 microM of lycopene in the dark for 2 h before exposure to UVA (22.5 KJ/m2). Then, DNA damage measured by the single-cell gel electrophoretic assay (comet assay) and the expression of HO-1 measured by western blotting were determined. In addition, we exposed lycopene powder to UVA (22.5 KJ/m2) to prepare pre-irradiated lycopene (ILP). Then, C3H cells were incubated with ILP for 2 h, and DNA damage and the expression of HO-1 also were determined.
  
  
  RESULTS
  We found that lycopene enrichment did not cause damage to DNA in C3H cells not irradiated with UVA. However, lycopene enrichment strongly induced DNA damage when cells were irradiated with UVA (by ca. 2-fold as compared to control). In addition, lycopene enhanced UVA-induced HO-1 expression by ca. 2.5-fold. UVA irradiation led to a significant loss of lycopene that had been pre-incorporated into C3H cells. When cells were incubated with lycopene that had been pre-irradiated with UVA without subjecting the cells to further UVA irradiation, cellular DNA damage and expression of HO-1 were markedly increased, and these effects of irradiated lycopene were concentration-dependent.
  
  
  CONCLUSIONS
  These results demonstrate that lycopene enhances UVA-induced oxidative stress in C3H cells, and they suggest that under UVA irradiation, lycopene may produce oxidative products that are responsible for the prooxidant effects.
authors.affiliation: Graduate Institute of Nutritional Science, Chung Shan Medical University, Taichung, Taiwan, ROC.
authors.forename: Shu-Lan
authors.initials: SL
authors.lastname: Yeh
authors.forename: Chin-Shiu
authors.initials: CS
authors.lastname: Huang
authors.forename: Miao-Lin
authors.initials: ML
authors.lastname: Hu
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002338:Carotenoids / Q000494:pharmacology*; D002470:Cell Survival; D002478:Cells, Cultured; D020552:Comet Assay; D004249:DNA Damage / Q000187:drug effects / Q000528:radiation effects; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects; D051547:Heme Oxygenase-1 / Q000378:metabolism*; D000077276:Lycopene; D051379:Mice; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D011837:Radiation-Protective Agents / Q000494:pharmacology*; D014466:Ultraviolet Rays / Q000009:adverse effects*
chemical_list: D011837:Radiation-Protective Agents; D002338:Carotenoids; D051547:Heme Oxygenase-1; D000077276:Lycopene