کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2515606 1118535 2007 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Involvement of reactive oxygen species on the apoptotic mechanism induced by IFN-α2b in rat preneoplastic liver
موضوعات مرتبط
علوم پزشکی و سلامت داروسازی، سم شناسی و علوم دارویی داروشناسی
پیش نمایش صفحه اول مقاله
Involvement of reactive oxygen species on the apoptotic mechanism induced by IFN-α2b in rat preneoplastic liver
چکیده انگلیسی

Interferon-α2b (IFN-α2b) is an important component in the preventive treatment of patients who have severe hepatic illness such as hepatitis B or C and hepatocarcinomas. In a previous work, using a rat liver preneoplastic model, we have demonstrated that IFN-α2b reduces the number and volume of altered hepatic foci (AHF) inducing apoptosis through a mechanism mediated by TGF-β1. In this study, the implication of hepatocytes redox status of IFN-α2b-treated preneoplastic liver in the TGF-β1-induced apoptotic death was analyzed. Results indicate that IFN-α2b induces hepatocytic TGF-β1 production and secretion by induction of reactive oxygen species (ROS) formation through the activation of a membrane bound NADPH oxidase complex. TGF-β1, in turn, reduces hepatocytes antioxidant defenses and induces programmed cell death. On the other hand, it was also demonstrated that treatment of rats with IFN-α2b plus a ROS scavenger such as ascorbic acid, abolishes the apoptotic effect of IFN-α2b in rat preneoplastic livers, leading to an increase of the foci volume. In conclusion, these findings strongly suggest that ROS have a fundamental role as signaling and/or regulator molecules in the IFN-α2b-induced apoptosis in hepatic preneoplastic cells.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical Pharmacology - Volume 73, Issue 11, 1 June 2007, Pages 1776–1785
نویسندگان
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