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Pathophysiological implications of redox regulation in liver ROS play a crucial role in the induction and progression of different liver diseases and evidence of oxidative stress has been detected in almost all the clinical and experimental conditions of chronic liver diseases with different etiology and progression rate of fibrosis.4,5,27 The pathogenesis of the damage involves all the cell types present in the liver (hepatocytes, Kppfer, stellate and endothelial liver cells) via apoptosis, necrosis, ischemia and regeneration, all processes leading to altered gene expression.4 The main sources of free radicals are represented by neutrophils, endotoxin-activated Kppfer cells, hepatocyte mitochondria and cytochrome P450 enzymes.6 The relevance of cellular redox imbalance in liver diseases is outlined by a number of studies in patients with viral or alcoholic liver diseases showing a correlation between liver damage and increase in pro-oxidant cellular markers such as malondialdehyde, 4-hydroxynonenal and their protein adducts, associated with a concomitant decrease of GSH, vitamin E, vitamin C, selenium, etc.4,28 These markers may contribute to monitor the degree of liver damage and the response to antiviral therapies

T.et al (2001a)

CORT, Corticosterone

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