首页> 外文期刊>Toxicology: An International Journal Concerned with the Effects of Chemicals on Living Systems >Protection against ultraviolet B-induced oxidative DNA damage in rabbit corneal-derived cells (SIRC) by 4-coumaric acid.
【24h】

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

机译:4-香豆酸对紫外线B诱导的兔角膜衍生细胞(SIRC)的氧化DNA损伤的保护作用。

获取原文
获取原文并翻译 | 示例
           

摘要

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 corneal-derived cells (SIRC) exposed to UV-B 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+/-1.2x10(-6) to 29+/-6.2x10(-6) dG, means+/-SE). When 10 microM 4-coumaric acid was added to the medium, 8-OHdG levels were similar to those of unexposed cells (16.8+/-0.8x10(-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 microM 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 microM 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.
机译:细胞暴露于紫外线B辐射(UV-B)会诱导产生活性氧(ROS),从而破坏细胞成分。自由基清除剂和抗氧化剂会干扰ROS的产生。我们测量了4-羟基香豆酸(一种天然多酚)在暴露于UV-B的兔角膜衍生细胞(SIRC)中氧化DNA损伤的标志物8-羟基-2'-脱氧鸟苷(8-OHdG)水平。辐照后8-OHdG的水平显着增加(P <0.01)(从12 +/- 1.2x10(-6)dG增至29 +/- 6.2x10(-6)dG,均值+/- SE)。当将10 microM 4-香豆酸添加到培养基中时,8-OHdG的水平类似于未暴露细胞的水平(16.8 +/- 0.8x10(-6)dG)。 UV-B照射将SIRC细胞中的超氧化物歧化酶(SOD)活性从0.29 +/- 0.6降低至0.15 +/- 0.04 mU / mg(均值+/- SE)。 10 microM 4-香豆酸的存在阻止了SOD活性的降低(0.20 +/- 0.05 mU / mg,P <0.05)。相反,与对照相比,暴露于UV-B的SIRC细胞具有更高水平的黄嘌呤氧化酶(XO)活性(分别为0.40 +/- 0.07和0.24 +/- 0.08 mU / mg,均值+/- SE)。在存在10 microM 4-香豆酸的情况下,可防止XO活性增加(0.16 +/- 0.03 mU / mg;平均值+/- SE)。总之,4-香豆酸抑制了UV-B诱导SIRC细胞中的氧化DNA损伤,4-香豆酸可能通过其自由基清除活性,稳定了SOD活性,并阻止了UV-B照射后XO活性的增加。因此,局部使用4-香豆酸可以防止角膜中的自由基损伤。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号