| Literature DB >> 17723268 |
Perla Deyanira Maldonado1, María Elena Chánez-Cárdenas, Diana Barrera, Juana Villeda-Hernández, Abel Santamaría, José Pedraza-Chaverrí.
Abstract
Reactive oxygen and nitrogen species formation leads to DNA damage in animals treated with quinolinic acid. Poly(ADP-ribose) polymerase-1 (PARP-1) is a protein involved in the DNA base excision repair system. Its overactivation promotes cellular energy deficit and necrosis. Here, we evaluated the effect of PJ-34, a potent inhibitor of PARP-1, on the neuronal damage induced by quinolinic acid. Animals were administered with PJ-34 (10 mg/kg, i.p.), 1 h before and 1 h after a striatal infusion of 1 microl of quinolinic acid (240 nmol). PJ-34 clearly attenuated the circling behavior produced by quinolinic acid and completely prevented the histological damage induced by the toxin. The protective effect of PJ-34 suggests that PARP-1 activation is playing an active role in the neuronal death induced by quinolinic acid.Entities:
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Year: 2007 PMID: 17723268 DOI: 10.1016/j.neulet.2007.08.013
Source DB: PubMed Journal: Neurosci Lett ISSN: 0304-3940 Impact factor: 3.046