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Ethanol Impaired Liver Regeneration is Associated with Increased Oxidative Stress and DNA Damage in Hepatocytes.
Author(s) -
Chaudhry Rajeev,
Duan Kevin,
Pang Maoyin,
Wands Jack,
Monte Suzanne
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a188-b
Subject(s) - oxidative stress , liver regeneration , steatosis , lipid peroxidation , dna damage , liver injury , regeneration (biology) , chemistry , ethanol , endocrinology , medicine , biochemistry , biology , microbiology and biotechnology , dna
Background: Ethanol inhibition of liver regeneration was shown to be mediated in part by impaired insulin signaling. However, ethanol also causes liver injury due to acetaldehyde production and oxidative stress. Objectives: This study utilizes an in vivo model to examine the role of oxidative stress and DNA damage in relation to ethanol impaired liver regeneration. Materials and Methods: Long‐Evans rats were fed liquid diets containing 0% or 37% ethanol by caloric content for 5 weeks. Rats were subjected to 70% hepatectomy. Livers were harvested to examine DNA synthesis, DNA damage, and oxidative stress. Results: Ethanol‐exposed livers had increased steatosis, lobular inflammation, and apoptosis, and their hepatocytes were smaller, and had poorly organized lobular architectures, and strikingly reduced BrdU labeling relative to control. In addition, immunohistochemcal staining and ELISA studies demonstrated that ethanol‐exposed livers had more abundant and widely distributed immunoreactivity for 8‐OHdG and HNE, reflecting increased DNA damage and lipid peroxidation. Conclusions: Ethanol impaired liver regeneration is associated with increased oxidative injury and DNA damage. Future studies will determine if ethanol‐induced oxidative stress also impairs insulin signaling during liver regeneration.