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细胞内氧化还原状态与氧化应激:对细胞增殖、凋亡及致癌作用的影响

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

作者信息

Matés José M, Segura Juan A, Alonso Francisco J, Márquez Javier

机构信息

Department of Biología Molecular y Bioquímica, Facultad de Ciencias, Campus de Teatinos, Universidad de Málaga, Málaga, Spain.

出版信息

Arch Toxicol. 2008 May;82(5):273-99. doi: 10.1007/s00204-008-0304-z. Epub 2008 Apr 29.

Abstract

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.

摘要

氧化应激可定义为细胞内氧化剂生成与抗氧化能力之间的失衡。活性氧(ROS)参与了从细胞凋亡、坏死到细胞增殖和致癌作用等多种不同的细胞过程。事实上,诸如诱导细胞增殖、减少细胞凋亡以及氧化性DNA损伤等分子事件已被认为在致癌过程中起着关键作用。致癌性和衰老具有一系列复杂的终点特征,这些特征表现为一系列分子反应。ROS可改变许多细胞内信号通路,包括蛋白磷酸酶、蛋白激酶和转录因子,这表明ROS的大多数作用是通过其对信号通路的作用,而非通过对大分子的非特异性损伤;然而,氧化还原状态诱导细胞增殖或死亡的确切机制,以及氧化应激如何导致引发肿瘤形成的过程仍在研究之中。

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