Abstract |
Poly(ADP-ribose) polymerase-1 (PARP-1) is involved in DNA repair, but its overactivation can induce cell death. Our aim was to investigate the role of PARP-1 in activation of programmed cell death processes in the brain during systemic inflammation. Our data indicated that lipopolysaccharide (1mg/kgb.w., i.p.)-evoked systemic inflammation enhanced PARP-1 activity in the mouse brain, leading to the lowering of beta- NAD(+) concentration, to translocation of apoptosis inducing factor from mitochondria to the nucleus, and to enhanced lipid peroxidation. Inhibitor of PARP-1, 3-aminobenzamide (30 mg/kgb.w., i.p.), protected the brain against prooxidative and cell death processes, suggesting involvement of PARP-1 in systemic inflammation-related processes in the brain.
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Authors | Grzegorz A Czapski, Magdalena Cakala, Barbara Gajkowska, Joanna B Strosznajder |
Journal | Neurochemistry international
(Neurochem Int)
Vol. 49
Issue 8
Pg. 751-5
(Dec 2006)
ISSN: 0197-0186 [Print] England |
PMID | 16904242
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Benzamides
- Lipopolysaccharides
- Poly(ADP-ribose) Polymerase Inhibitors
- 3-aminobenzamide
- Parp1 protein, mouse
- Poly (ADP-Ribose) Polymerase-1
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Topics |
- Animals
- Benzamides
(pharmacology)
- Brain
(drug effects, enzymology, ultrastructure)
- Inflammation
(enzymology)
- Lipopolysaccharides
(pharmacology)
- Mice
- Microscopy, Electron
- Poly (ADP-Ribose) Polymerase-1
- Poly(ADP-ribose) Polymerase Inhibitors
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