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Titolo:
Effects of the nitrone radical scavengers PBN and S-PBN on in vivo trapping of reactive oxygen species after traumatic brain injury in rats
Autore:
Marklund, N; Lewander, T; Clausen, F; Hillered, L;
Indirizzi:
Univ Uppsala Hosp, Dept Neurosci, SE-75185 Uppsala, Sweden Univ Uppsala Hosp Uppsala Sweden SE-75185 osci, SE-75185 Uppsala, Sweden Univ Uppsala Hosp, Dept Neurosurg, SE-75185 Uppsala, Sweden Univ Uppsala Hosp Uppsala Sweden SE-75185 surg, SE-75185 Uppsala, Sweden Univ Uppsala Hosp, Dept Psychiat, Ulleraker, SE-75185 Uppsala, Sweden UnivUppsala Hosp Uppsala Sweden SE-75185 aker, SE-75185 Uppsala, Sweden Univ Uppsala Hosp, Dept Med Sci, SE-75185 Uppsala, Sweden Univ Uppsala Hosp Uppsala Sweden SE-75185 Sci, SE-75185 Uppsala, Sweden
Titolo Testata:
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
fascicolo: 11, volume: 21, anno: 2001,
pagine: 1259 - 1267
SICI:
0271-678X(200111)21:11<1259:EOTNRS>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
TERT-BUTYL-NITRONE; COMPRESSION CONTUSION TRAUMA; FOCAL CEREBRAL-ISCHEMIA; NERVOUS-SYSTEM TRAUMA; NITRIC-OXIDE SYNTHASE; LIPID-PEROXIDATION; ALPHA-PHENYLNITRONE; ENDOTHELIAL-CELLS; OXIDATIVE STRESS; HEAD-INJURY;
Keywords:
4-hydroxybenzoic acid; nitrone PBN radical; rats; reactive oxygen species; S-PBN; traumatic brain injury;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
66
Recensione:
Indirizzi per estratti:
Indirizzo: Marklund, N Univ Uppsala Hosp, Dept Neurosci, SE-75185 Uppsala, Sweden Univ Uppsala Hosp Uppsala Sweden SE-75185 85 Uppsala, Sweden
Citazione:
N. Marklund et al., "Effects of the nitrone radical scavengers PBN and S-PBN on in vivo trapping of reactive oxygen species after traumatic brain injury in rats", J CEREBR B, 21(11), 2001, pp. 1259-1267

Abstract

In previous studies, the authors showed that the nitrone radical scavengeralpha -phenyl-N-tert-butyl nitrone (PBN) and its sulfo-derivative, 2-sulfo-phenyl-N-tert-butyl nitrone (S-PBN), attenuated cognitive disturbance and reduced tissue damage after traumatic brain injury (TBI) in rats. In the current study, the production of reactive oxygen species (ROS) after TBI was monitored with microdialysis and the 4-hydroxybenzoic acid (4-HBA) trappingmethod. A single dose of PBN (30 mg/kg) or an equimolar dose of S-PBN (47 mg/kg) was administered intravenously 30 minutes before a controlled cortical contusion injury in rats. Plasma and brain tissue drug concentrations were analyzed at the end of the microdialysis experiment (3 hours after injury) and, in a separate experiment with S-PBN, at 30 and 60 minutes after injury. Traumatic brain injury caused a significant increase in ROS formation that lasted for 60 minutes after the injury as evidenced by increased 3,4-dihydroxybenzoic acid (3,4-DHBA) concentrations in the dialysate. PBN and S-PBN equally and significantly attenuated the posttraumatic increase in 3,4-DHBA formation. High PBN concentrations were found bilaterally in brain tissue up to 3 hours after injury. In contrast, S-PBN was rapidly cleared fromthe circulation and was not detectable in brain at 30 minutes after injuryor at any later time point. The results suggest that scavenging of ROS after TBI may contribute to the neuroprotective properties observed with nitrone spin-trapping agents. S-PBN, which remained undetectable even in traumatized brain tissue, reduced ROS production to the same extent as PBN that readily crossed the blood-brain barrier. This finding supports an important role for ROS production at the blood-endothelial interface in TBI.

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Documento generato il 08/08/20 alle ore 00:13:03