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Paraoxonase 1 and oxidative stress in paediatric non-alcoholic steatohepatitis

Authors

  • Sonal Desai,

    1. Women and Children's Hospital of Buffalo, Department of Pediatrics, the State University of New York, Buffalo, NY, USA
    Current affiliation:
    1. Division of Gastroenterology Hepatology and Nutrition, Department of Pediatrics, University of Texas Health Science Center San Antonio, San Antonio, TX, USA
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  • Susan S. Baker,

    1. Women and Children's Hospital of Buffalo, Department of Pediatrics, the State University of New York, Buffalo, NY, USA
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  • Wensheng Liu,

    1. Women and Children's Hospital of Buffalo, Department of Pediatrics, the State University of New York, Buffalo, NY, USA
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  • Diana A. Moya,

    1. Women and Children's Hospital of Buffalo, Department of Pediatrics, the State University of New York, Buffalo, NY, USA
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  • Richard W. Browne,

    1. Department of Biotechnical and Clinical Laboratory Sciences, the State University of New York at Buffalo, Buffalo, NY, USA
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  • Lucy Mastrandrea,

    1. Women and Children's Hospital of Buffalo, Department of Pediatrics, the State University of New York, Buffalo, NY, USA
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  • Robert D. Baker,

    1. Women and Children's Hospital of Buffalo, Department of Pediatrics, the State University of New York, Buffalo, NY, USA
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  • Lixin Zhu

    Corresponding author
    1. Women and Children's Hospital of Buffalo, Department of Pediatrics, the State University of New York, Buffalo, NY, USA
    • Correspondence

      Lixin Zhu, Digestive Diseases and Nutrition Center, Department of Pediatrics, the State University of New York at Buffalo, 3435 Main Street, 422BRB, Buffalo, NY14214, USA

      Tel: +1716 829 2191

      Fax: +1716 829 3585

      e-mail: lixinzhu@buffalo.edu

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Abstract

Background & Aims

Non-alcoholic steatohepatitis (NASH) in children is a significant public health concern. Oxidative stress is an important component in the pathophysiology of NASH. Several enzymatic antioxidant mechanisms protect the liver from oxidative injury. Examination of the expression of these enzymes in NASH livers may provide insight on the roles for these antioxidant mechanisms in the pathophysiology of NASH.

Methods

The mRNA expression of catalase, glutathione peroxidase 1 (GPX1), glutathione reductase (GSR), paraoxonase 1 (PON1) and other reactive oxygen species-related genes was evaluated by microarray and quantitative real-time PCR analyses. The PON1 protein levels were evaluated in liver and serum by Western blot analyses. Serum enzymatic activities of GPX, GSR and PON1 (paraoxonase and arylesterase activities) were examined.

Results

NASH livers exhibited elevated mRNA expression of catalase and PON1, but not GPX1 or GSR. No difference in serum GPX or GSR activity was detected between NASH patients and controls. Elevated expression of PON1 mRNA and protein was detected in NASH livers, but serum PON1 protein and activities were not elevated.

Conclusions

Elevated expression of catalase and PON1 suggests protective roles for these antioxidants in NASH livers. Given the importance of oxidative stress in the pathophysiology of NASH, future studies focusing on these enzymes could identify important targets for therapeutic or preventive interventions for NASH patients.

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