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首页> 外文期刊>Molecular Nutrition and Food Research >Impact of copper on the induction and repair of oxidative DNA damage, poly(ADP-ribosyl)ation and PARP-1 activity.
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Impact of copper on the induction and repair of oxidative DNA damage, poly(ADP-ribosyl)ation and PARP-1 activity.

机译：铜对诱导和修复氧化DNA损伤，聚（ADP-核糖基）和PARP-1活性的影响。

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摘要

Copper is an essential trace element involved, among other functions, in enzymatic antioxidative defense systems. However, nonprotein bound copper ions have been shown to generate reactive oxygen species. To gain insight into the discrepancy between the protective properties of copper on the one hand and its toxicity on the other hand, we examined the genotoxic effects of CuSO4 in cultured human cells. Here we report that copper, at cytotoxic concentrations, induces oxidative DNA base modifications and DNA strand breaks. However, at lower noncytotoxic concentrations, copper inhibits the repair of oxidative DNA damage induced by visible light. As a first mechanistic hint, inhibition of H2O2-induced poly(ADP-ribosyl)ation was identified in cultured cells and further experiments demonstrated a strong inhibition of the activity of isolated poly(ADP-ribose)polymerase-1 (PARP-1) by copper. Bioavailability studies of copper showed a dose-dependent uptake in cells and pointed out the relevance of the applied concentrations. Taken together, the results indicate that copper, under conditions of either disturbed homeostasis or overload due to high exposure, exerts defined genotoxic effects. Hence, a balance needs to be maintained to ensure sufficient uptake and to prevent overload..
机译：铜是酶抗氧化防御系统中不可或缺的微量元素。然而，已经证明非蛋白质结合的铜离子会产生活性氧。为了一方面了解铜的保护特性与另一方面的毒性之间的差异，我们研究了CuSO4在培养的人细胞中的遗传毒性作用。在这里，我们报道铜以细胞毒性浓度诱导氧化性DNA碱基修饰和DNA链断裂。然而，在较低的非细胞毒性浓度下，铜抑制了可见光诱导的氧化性DNA损伤的修复。作为第一个机制提示，在培养的细胞中鉴定出H2O2诱导的聚（ADP-核糖）聚合酶的抑制作用，并且进一步的实验表明，H2O2诱导的分离的聚（ADP-核糖）聚合酶-1（PARP-1）的活性受到强烈抑制。铜。铜的生物利用度研究显示细胞中剂量依赖性吸收，并指出了所应用浓度的相关性。两者合计，结果表明，铜在由于高度暴露而导致的稳态不稳定或过载的情况下，发挥了明确的遗传毒性作用。因此，需要保持平衡以确保足够的摄取并防止过载。

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