Yeh Shu-Lan, Huang Chin-Shiu, Hu Miao-Lin
Graduate Institute of Nutritional Science, Chung Shan Medical University, Taichung, Taiwan, ROC.
Eur J Nutr. 2005 Sep;44(6):365-70. doi: 10.1007/s00394-004-0536-5. Epub 2004 Nov 18.
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.
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.
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.
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.
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.
有研究表明，包括番茄红素在内的类胡萝卜素可能降低光损伤风险。然而，类胡萝卜素在光照下不稳定，在某些情况下可能产生促氧化作用。
我们研究了番茄红素是否能抑制紫外线A（UVA）诱导的DNA损伤和血红素加氧酶-1（HO-1）的表达。我们假设UVA照射导致的番茄红素分解，而非完整的番茄红素本身，会引起氧化损伤。
小鼠成纤维细胞C3H10T1/2（C3H）首先在黑暗中用10微摩尔番茄红素富集2小时，然后暴露于UVA（22.5千焦/平方米）。然后，通过单细胞凝胶电泳分析（彗星试验）测量DNA损伤，并通过蛋白质印迹法测定HO-1的表达。此外，我们将番茄红素粉末暴露于UVA（22.5千焦/平方米）以制备预照射番茄红素（ILP）。然后，将C3H细胞与ILP孵育2小时，并测定DNA损伤和HO-1的表达。
我们发现，在未接受UVA照射的C3H细胞中，番茄红素富集不会对DNA造成损伤。然而，当细胞接受UVA照射时，番茄红素富集强烈诱导DNA损伤（与对照组相比约增加2倍）。此外，番茄红素使UVA诱导的HO-1表达增加约2.5倍。UVA照射导致预先掺入C3H细胞的番茄红素显著损失。当细胞与预先用UVA照射的番茄红素孵育而不使细胞进一步接受UVA照射时，细胞DNA损伤和HO-1表达明显增加，且照射后番茄红素的这些作用呈浓度依赖性。
这些结果表明，番茄红素增强了UVA诱导的C3H细胞氧化应激，提示在UVA照射下，番茄红素可能产生导致促氧化作用的氧化产物。
