Nitric oxide and redox regulation in the liver: part II. Redox biology in pathologic hepatocytes and implications for intervention.
Nitric oxide and redox regulation in the liver: part II. Redox biology in pathologic hepatocytes and implications for intervention.
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DOI：
10.1016/j.jss.2009.10.006
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发表时间：
2011-05-01
期刊：
影响因子：
--
通讯作者：
Kuo PC
中科院分区：
文献类型：
--
作者：
Diesen DL;Kuo PC
活性氧 (ROS) 和活性氮 (RNS) 在正常肝细胞中产生，对于氧化呼吸、生长、再生、细胞凋亡和微粒体防御等正常生理过程至关重要。当氧化产物的水平超过正常抗氧化系统的能力时，就会发生氧化应激。这种以 ROS 和 RNS 形式存在的应激，可通过诱导炎症、缺血、纤维化、坏死、凋亡，或通过破坏脂质、蛋白质和/或 DNA 导致恶性转化，损害所有肝细胞，包括肝细胞、库普弗细胞、星状细胞和内皮细胞。在本综述的第一部分中，我们将讨论肝脏中的基本氧化还原生物学，包括对 ROS、RNS 和抗氧化剂的综述，重点关注作为 RNS 常见来源的一氧化氮。然后，我们将回顾氧化应激作为肝炎（酒精性、病毒性、非酒精性）肝损伤机制的证据。在本综述的第二部分中，我们将回顾常见病理生理条件下的氧化应激，包括缺血/再灌注损伤、纤维化、肝细胞癌、铁超载、威尔逊病、脓毒症和对乙酰氨基酚过量。最后，生物标志物、蛋白质组学和抗氧化疗法将作为未来治疗干预的领域进行讨论。
Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are created in normal hepatocytes and are critical for normal physiological processes including oxidative respiration, growth, regeneration, apoptosis, and microsomal defense. When the levels of oxidation products exceed the capacity of normal antioxidant systems, oxidative stress occurs. This type of stress, in the form of ROS and RNS, can be damaging to all liver cells, including hepatocytes, Kupffer cells, stellate cells, and endothelial cells, through induction of inflammation, ischemia, fibrosis, necrosis, apoptosis, or through malignant transformation by damaging lipids, proteins, and/or DNA. In part I of this review, we will discuss basic redox biology in the liver, including a review of ROS, RNS, and antioxidants, with a focus on nitric oxide as a common source of RNS. We will then review the evidence for oxidative stress as a mechanism of liver injury in hepatitis (alcoholic, viral, non-alcoholic). In part II of this review, we will review oxidative stress in common pathophysiological conditions including ischemia/reperfusion injury, fibrosis, hepatocellular carcinoma, iron overload, Wilson’s disease, sepsis and acetaminophen overdose. Finally, biomarkers, proteomic, and antioxidant therapies will be discussed as areas for future therapeutic interventions.
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DOI：
10.1152/ajpheart.01173.2005
发表时间：
2006-12-01
影响因子：
4.8
作者：
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