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Intracellular redox status and oxidative stress: implications for cell proliferation, apoptosis, and carcinogenesis.

机译:细胞内氧化还原状态和氧化应激:对细胞增殖,凋亡和致癌作用的影响。

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摘要

Oxidative stress can be defined as the imbalance between cellular oxidant species production and antioxidant capability. Reactive oxygen species (ROS) are involved in a variety of different cellular processes ranging from apoptosis and necrosis to cell proliferation and carcinogenesis. In fact, molecular events, such as induction of cell proliferation, decreased apoptosis, and oxidative DNA damage have been proposed to be critically involved in carcinogenesis. Carcinogenicity and aging are characterized by a set of complex endpoints, which appear as a series of molecular reactions. ROS can modify many intracellular signaling pathways including protein phosphatases, protein kinases, and transcription factors, suggesting that the majority of the effects of ROS are through their actions on signaling pathways rather than via non-specific damage of macromolecules; however, exact mechanisms by which redox status induces cells to proliferate or to die, and how oxidative stress can lead to processes evoking tumor formation are still under investigation.
机译:氧化应激可以定义为细胞氧化剂种类产生和抗氧化能力之间的不平衡。活性氧(ROS)参与了许多不同的细胞过程,从细胞凋亡和坏死到细胞增殖和癌变。实际上,已经提出了分子事件,例如诱导细胞增殖,细胞凋亡减少和DNA氧化损伤,都与致癌作用密切相关。致癌性和衰老的特征是一系列复杂的终点,这些终点表现为一系列分子反应。 ROS可以修饰许多细胞内信号传导途径,包括蛋白质磷酸酶,蛋白激酶和转录因子,这表明ROS的大部分作用是通过其对信号传导途径的作用,而不是通过大分子的非特异性损伤来实现的;但是,氧化还原状态诱导细胞增殖或死亡以及氧化应激如何导致诱发肿瘤形成过程的确切机制仍在研究中。

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