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  • Title: PARP-1-dependent 3-nitrotyrosine protein modification after DNA damage.
    Author: Siles E, Martinez-Lara E, Núñez MI, Muñoz-Gámez JA, Martín-Oliva D, Valenzuela MT, Peinado MA, Ruiz de Almodóvar JM, Javier Oliver F.
    Journal: J Cell Biochem; 2005 Nov 01; 96(4):709-15. PubMed ID: 16052507.
    Abstract:
    3-nitrotyrosine (NO2-Tyr) is thought to be a specific marker of cell injury during oxidative damage. We have evaluated the role of poly(ADP-ribose)polymerase-1 (PARP-1) in protein nitration after treatment of immortalized fibroblasts parp-1+/+ and parp-1-/- with the alkylating agent 2'-methyl-2'-nitroso-urea (MNU). Both cell lines showed increased iNOS expression following MNU treatment in parallel with a selective induction of tyrosine nitration of different proteins. PARP-1 deficient cells displayed a delayed iNOS accumulation, reduced number of nitrated proteins, and a lower global nitrotyrosine "footprint." We have identified the mitochondrial compartment as the major site of oxidative stress during DNA damage, being MnSOD one of the NO2-Tyr-modified proteins, but not in parp-1-/- cells. These results suggest that NO-derived injury can be modulated by proteins involved in the response to genotoxic damage, such as PARP-1, and may account for the limited oxidative injury in parp-1 knockout mice during carcinogenesis and inflammation.
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