氧化应激
致癌物
表观遗传学
肝细胞癌
活性氧
DNA损伤
炎症
突变
机制(生物学)
氧化磷酸化
癌症研究
生物
细胞生物学
化学
遗传学
免疫学
生物化学
基因
DNA
哲学
认识论
作者
Mirko Tarocchi,Andrea Galli
出处
期刊:Elsevier eBooks
[Elsevier]
日期:2017-01-01
卷期号:: 279-287
被引量:6
标识
DOI:10.1016/b978-0-12-804274-8.00021-7
摘要
More than 700,000 new cases of hepatocellular carcinoma (HCC) are diagnosed every year in the world. Many different etiological factors can induce hepatic damage and promote the hepatocarcinogenic process. Among virus infections, metabolic disorder, or genetic mutation, the mechanisms underlying these processes are heterogeneous, but inflammation and oxidative stress seem to be a common pattern. Indeed, chronic oxidative stress in the hepatic parenchyma induces the accumulation of reactive oxygen species (ROS) and other radicals that react with lipids, protein, and even DNA. The alteration of the normal cellular functions, the activation of different pathways, the epigenetic alteration, and the direct and indirect induction of genetic mutation are all effects of the oxidative stress; all of these generate a favorable environment for the carcinogenic process.
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