School of Bioresources Science, Andong National University, Andong, Republic of Korea.
Cancer Lett. 2010 Jul 1;293(1):58-64. doi: 10.1016/j.canlet.2009.12.019. Epub 2010 Jan 18.
Oxidative DNA damage is the most critical factor implicated in carcinogenesis and other disorders. However, the protective effects of lunasin against oxidative DNA damage have not yet reported. In this study, we report here the protective effect of lunasin purified from Solanum nigrum L. against oxidative DNA. Lunasin protected DNA from the oxidative damage induced by Fe(2+) ion and hydroxyl radical. To better understand the mechanism for the protective effect of lunasin against DNA damage, the abilities to chelate Fe(2+), scavenge the generated hydroxyl radical and block the generation of hydroxyl radical were evaluated. Although it did not scavenge generated hydroxyl radical, lunasin blocked the generation of hydroxyl radical by chelating Fe(2+) ion. We conclude that lunasin protects DNA from oxidation by blocking fenton reaction between Fe(2+) and H(2)O(2) by chelating Fe(2+) and that consumption of lunasin may play an important role in the chemoprevention for the oxidative carcinogenesis.
氧化 DNA 损伤是致癌作用和其他疾病中最关键的因素。然而,亮抑酶肽对氧化 DNA 损伤的保护作用尚未见报道。在这项研究中,我们报告了从茄属植物中纯化的亮抑酶肽对氧化 DNA 的保护作用。亮抑酶肽可防止 Fe(2+)离子和羟自由基诱导的 DNA 氧化损伤。为了更好地理解亮抑酶肽对 DNA 损伤的保护作用机制,评估了亮抑酶肽螯合 Fe(2+)、清除生成的羟自由基和阻断羟自由基生成的能力。尽管亮抑酶肽不能清除生成的羟自由基,但它通过螯合 Fe(2+)离子阻断了 Fenton 反应中羟自由基的生成。我们得出结论,亮抑酶肽通过螯合 Fe(2+)阻断 Fenton 反应(Fe(2+)与 H(2)O(2)之间的反应)从而保护 DNA 免受氧化,亮抑酶肽的消耗可能在氧化致癌的化学预防中发挥重要作用。