Serum Xanthine Oxidase in Human Liver Disease

Battelli, Maria Giulia; Musiani, S; Valgimigli, Marco; Gramantieri, Laura; Tomassoni, Federica; Bolondi, Luigi; Stirpe, Fiorenzo

doi:10.1111/j.1572-0241.2001.03700.x

Cited by 53 publications

(32 citation statements)

References 30 publications

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“…In this study, the serum TC level decreased slightly and the serum TBA level increased slightly in EEFP-treated female group (1.875 g/kg/d), which may be because the transformation from TC to TBA was increased by EEFP. Elevation of serum XOD activity in patients with chronic liver disease seems to reflect the presence of cholestasis (Battelli et al, 2001). In our study, the serum XOD activity increased in EEFP-treated male group (1.25 g/kg/d) and all EEFPtreated female groups, suggesting that EEFP could induce cholestasis.…”

Section: Discussionmentioning

confidence: 86%

Evaluation of hepatotoxicity and cholestasis in rats treated with EtOH extract of Fructus Psoraleae

Wang

Jiang

et al. 2012

Journal of Ethnopharmacology

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Section: Discussionmentioning

confidence: 86%

Evaluation of hepatotoxicity and cholestasis in rats treated with EtOH extract of Fructus Psoraleae

Wang

Jiang

et al. 2012

Journal of Ethnopharmacology

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“…XO released from the ailing liver is a major source of ROS [49]. Because an increase in XO activity was found in BDL rats, allopurinol, a XO inhibitor, was investigated as an antioxidant (oxidant inhibitor) treatment.…”

Section: Discussionmentioning

confidence: 99%

Systemic oxidative stress is implicated in the pathogenesis of brain edema in rats with chronic liver failure

Bosoi

Yang

Huynh

et al. 2012

Free Radical Biology and Medicine

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Chronic liver failure leads to hyperammonemia, a central component in the pathogenesis of hepatic encephalopathy (HE); however, a correlation between blood ammonia levels and HE severity remains controversial. It is believed oxidative stress plays a role in modulating the effects of hyperammonemia. This study aimed to determine the relationship between chronic hyperammonemia, oxidative stress, and brain edema (BE) in two rat models of HE: portacaval anastomosis (PCA) and bile-duct ligation (BDL). Ammonia and reactive oxygen species (ROS) levels, BE, oxidant and antioxidant enzyme activities, as well as lipid peroxidation were assessed both systemically and centrally in these two different animal models. Then, the effects of allopurinol (xanthine oxidase inhibitor, 100 mg/kg for 10 days) on ROS and BE and the temporal resolution of ammonia, ROS, and BE were evaluated only in BDL rats. Similar arterial and cerebrospinal fluid ammonia levels were found in PCA and BDL rats, both significantly higher compared to their respective sham-operated controls (p < 0.05). BE was detected in BDL rats (p < 0.05) but not in PCA rats. Evidence of oxidative stress was found systemically but not centrally in BDL rats: increased levels of ROS, increased activity of xanthine oxidase (oxidant enzyme), enhanced oxidative modifications on lipids, as well as decreased antioxidant defense. In PCA rats, a preserved oxidant/antioxidant balance was demonstrated. Treatment with allopurinol in BDL rats attenuated both ROS and BE, suggesting systemic oxidative stress is implicated in the pathogenesis of BE. Analysis of ROS and ammonia temporal resolution in the plasma of BDL rats suggests systemic oxidative stress might be an important "first hit", which, followed by increases in ammonia, leads to BE in chronic liver failure. In conclusion, chronic hyperammonemia and oxidative stress in combination lead to the onset of BE in rats with chronic liver failure. HIGHLIGHTS► Hyperammonemia does not lead independently to brain edema in chronic liver failure. ► Systemic oxidative stress plays a role in brain edema in chronic liver failure. ► Systemic oxidative stress induces brain edema synergistically with hyperammonemia. ► Systemic oxidative stress is an important "first hit" in chronic liver failure.

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“…Liver-derived oxidant xanthine oxidase intervenes in the purine metabolism by oxidizing hypoxanthine to xanthine, and xanthine to uric acid, reactions which lead to H2O2 release. Xanthine oxidase activity in plasma has been demonstrated to be increased in cirrhotic patients (Battelli et al 2001). Therefore, inhibiting this enzyme with the hypoxanthine analog allopurinol significantly attenuates plasmatic oxidative stress (Spahr et al 2007).…”

Section: Sources Of Oxidative Stress In Cirrhosismentioning

confidence: 99%

Oxidative stress: a systemic factor implicated in the pathogenesis of hepatic encephalopathy

Bosoi

Rose

2012

Metab Brain Dis

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Serum Xanthine Oxidase in Human Liver Disease

Abstract: A marked elevation of serum XO in patients with chronic liver disease seems to reflect the presence of cholestasis. No correlation between XO levels and histological or serum evidence of hepatocyte necrosis was found in these patients.

Cited by 53 publications

References 30 publications

Evaluation of hepatotoxicity and cholestasis in rats treated with EtOH extract of Fructus Psoraleae

Evaluation of hepatotoxicity and cholestasis in rats treated with EtOH extract of Fructus Psoraleae

Systemic oxidative stress is implicated in the pathogenesis of brain edema in rats with chronic liver failure

Oxidative stress: a systemic factor implicated in the pathogenesis of hepatic encephalopathy

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