Linked Life Data

9591618

Source:http://linkedlifedata.com/resource/pubmed/id/9591618

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1998-6-25
pubmed:abstractText
The neuronal origins and mechanisms of central nervous system oxygen toxicity are only partly understood. Oxygen free radicals are felt to play a major role in the production of CNS oxygen toxicity because of the interactions of free radicals with plasma membranes producing lipid peroxidation. The cytochrome P-450 monooxygenase system IIE1 isozyme is important in the brain. This led to trials of P450 monooxygense inhibitors for prevention of oxygen toxicity. Diethyldithiocarbonate (DDC) proved to be the most promising agent in this class; 21-aminosteroid lazeroid compounds have been successful in experimentally limiting pulmonary oxygen toxicity. This led to our trying to prevent neuronal oxygen toxicity by the use of 21-aminosteroid and six other drugs during hyperoxia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0095-6562
pubmed:author
pubmed:issnType
Print
pubmed:volume
69
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
480-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Use of cytochrome-P450 mono-oxygenase 2 E1 isozyme inhibitors to delay seizures caused by central nervous system oxygen toxicity.
pubmed:affiliation
Dept. of Neurology, Medical College of Wisconsin, Milwaukee 53226, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't