Ethanol Treatment Up Regulates the Expression of Mitochondrial Manganese Superoxide Dismutase in Rat Liver

1994 ◽  
Vol 201 (3) ◽  
pp. 1356-1365 ◽  
Author(s):  
O.R. Koch ◽  
M.E. Deleo ◽  
S. Borrello ◽  
G. Palombini ◽  
T. Galeotti
1996 ◽  
Vol 220 (3) ◽  
pp. 546-552 ◽  
Author(s):  
Silvia Borrello ◽  
Maria Emilia De Leo ◽  
Matteo Landriscina ◽  
Bernardetta Palazzotti ◽  
Tommaso Galeotti

2005 ◽  
Vol 186 (3) ◽  
pp. 539-547 ◽  
Author(s):  
Virginia Fernández ◽  
Gladys Tapia ◽  
Patricia Varela ◽  
Iván Castillo ◽  
Catalina Mora ◽  
...  

Recently, we demonstrated that 3,3′,5-triiodothyronine (T3) induces oxidative stress in rat liver, with enhancement in the DNA binding of nuclear factor-κB (NF-κB) and the NF-κB-dependent expression of tumor necrosis factor-α (TNF-α). In this study, we show that T3 administration (daily doses of 0.1 mg/kg i.p. for three consecutive days) elicited a calorigenic response and higher liver O2 consumption rates, with increased serum levels of TNF-α (ELISA), liver inhibitor of κB (IκB-α) phosphorylation (Western blot analysis), and hepatic NF-κB DNA binding (EMSA) at 56–72 h after treatment. Within this time interval, liver manganese superoxide dismutase (MnSOD) activity and the protein expression of MnSOD and Bcl-2 are enhanced. These changes are abrogated by the administration of α-tocopherol (100 mg/kg i.p.) prior to T3. It is concluded that T3 treatment leads to the redox upregulation of MnSOD and Bcl-2 in rat liver, in association with TNF-α release and activation of the IκB-α kinase/NF-κB cascade, which may constitute a protective mechanism against free radical toxicity involving cell death signaling.


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