Abstract

While the exact ammonia-induced pathogenic mechanisms in hepatic encephalopathy (HE) are not completely understood, an increasing number of reports have lately been involved in studying the possible relevance of oxidative stress status in HE. Here we evaluated the levels of some oxidative stress markers (two main antioxidant enzymes: superoxide dismutase-SOD and glutathione peroxidase-GPX, as well as a lipid peroxidation marker: malondialdehyde-MDA) in thirty-six cirrhotic patients with overt HE (n=12) or minimal HE (n=24), as compared to a control age-matched group (n=19). We also included a group with cirrhosis without HE (n=42). Our results provide additional evidences of increased oxidative stress in both overt and minimal HE, as expressed by altered serum glutathione peroxidase antioxidant activity and increased levels of lipid peroxidation. Moreover, we demonstrated a significant correlation between the levels of the aforementioned oxidative stress markers and the severity of cirrhosis according to the Child and MELD scales, as well as with the venous blood ammonia level.

Highlights

  • While it is generally accepted that ammonia plays a central role in the pathogenic aspects involved in hepatic encephalopathy (HE) (Hazell et al, 1999), the exact mechanisms of its neurotoxicity remain poorly understood.Oxidative stress, which is the condition arising from an imbalance between toxic reactive oxygen species (ROS) and antioxidant systems (Sies, 1997), has been reported to be implicated in the development and the progression of various pathological conditions (Halliwell and Gutteridge, 2007), including acute and chronic liver diseases

  • Post-hoc comparisons showed a significant increase in Superoxide dismutase (SOD) activity in overt HE group (p

  • When we performed the post-hoc analysis, we observed a significant decrease in glutathione peroxidase (GPX) specific activity in overt HE (p=0.003), minimal HE (p=0.002) and the non-HE group (p=0.003), as compared to the controls

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Summary

Introduction

Oxidative stress, which is the condition arising from an imbalance between toxic reactive oxygen species (ROS) and antioxidant systems (Sies, 1997), has been reported to be implicated in the development and the progression of various pathological conditions (Halliwell and Gutteridge, 2007), including acute and chronic liver diseases. In this way, a previous number of studies have focused on the role of oxidative stress in liver injury (Chojkier et al, 1989, Yasa et al, 1999, Chen et al, 1997, Bhandari et al, 2008, Cesaratto et al, 2004). There are very few studies regarding these aspects in human patients, only related to alcohol poisoning-induced oxidative stress status in HE (Negru et al, 1999).

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