Linked Life Data

8711517

Source:http://linkedlifedata.com/resource/pubmed/id/8711517

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1996-9-6
pubmed:abstractText
Anesthetized rats were ventilated artificially to 10.5%-11.0% O2 in N2 (equivalent to altitude about 5 000 m). PBN (alpha-phenyl-ter-butylnitrone) was injected intravenously 5 min before hypoxia. The experiment results showed that the ESR (electron spin resonance) signal intensity of PBN-spin adduct in cortex and hippocampus both increased significantly during hypoxia (15 min) as compared with normoxia group (n = 5, P < 0.01). In the third group of rats injected with MPEG-SOD (monomethoxy-polyethylene glycol-superoxide dismutase) intravenously 20 min before hypoxia, the ESR signal intensity of PBN-spin adduct in cortex and hippocampus did not decrease significantly under hypoxia for 15 min (compared with hypoxia group, n = 5, P > 0.05). This may be due to the fact that MPEG-SOD could not pass the blood-brain barrier owing to its large molecular weight. The enzyme activity of SOD (superoxide dismutase. EC 1.15.1.1), GSH-Px (Glutathione peroxidase, EC 1.11.1.9) and content of MDA (malondialdehyde) was also determined. The results showed that the hypoxia had no effect on the SOD, GSH-Px activity and MDA content (n = 7 or n = 8, P > 0.05). The above results suggested that ventilation to 10.5%-11.0% O2 in N2 15 min induced free radical generation in rat's cortex and hippocampus, but this generation was not due to decrease of SOD, GSH-Px activity in cortex and hippocampus.
pubmed:language
chi
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0371-0874
pubmed:author
pubmed:issnType
Print
pubmed:volume
47
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
510-4
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
[Acute hypoxia induce free radicals generation in rat's cortex and hippocampus].
pubmed:affiliation
Shanghai Instiute of Physiology, Chinese Academy of Sciences.
pubmed:publicationType
Journal Article, English Abstract, Research Support, Non-U.S. Gov't