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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Role of oxidative stress in the increased activation of signal transducers and activators of transcription-3 in the fatty livers of obese Zucker rats.

BACKGROUND: Fatty livers have chronic oxidative stress, which could activate several transcription factors. We hypothesized that fatty livers of obese rats have increased activation of signal transducers and activators of transcription-1 and transcription-3 (Stat-1 and Stat-3) and that tocopherol treatment will decrease Stat activation. METHODS: Obese (Ob) and lean (Ln) Zucker rats with or without tocopherol treatment were used. Western blots of liver nuclear and cytoplasmic extracts to assess phosphorylated and total Stat-3 and tyrosine kinases Jak-2 and Tyk-2, immunohistochemistry to assess distribution of phosphoStat-3, and gel shift assays to assess Stat and nuclear factor kappa B binding were performed. Interleukin-6 serum levels and hepatic transcripts were determined by immunoassay and reverse polymerase chain reaction with Southern blotting, respectively. RESULTS: Livers of Ob animals had increased nuclear phosphoStat-3, decreased cytoplasmic Stat-3, and increased Stat-3 binding. Serum interleukin-6 was not measurable in either Ob or Ln animals and hepatic transcript levels were not significantly different. Tocopherol administration decreased nuclear phosphoStat-3, increased cytoplasmic Stat-3, and decreased Stat-3 binding activity. CONCLUSIONS: Chronic oxidative stress in fatty livers is associated with increased Stat-3 activation and decreased cytosolic Stat-3. Tocopherol treatment decreases Stat-3 activation and increases cytosolic Stat-3. Tocopherol-induced changes in Stat-3 may play a role in its beneficial effects in hepatic ischemia in fatty livers.[1]


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