Linked Life Data

3426233

Source:http://linkedlifedata.com/resource/pubmed/id/3426233

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1988-2-8
pubmed:abstractText
Measurement of both chemiluminescence (CL) and the formation of 2-thiobarbituric acid-reacting substances (TBAR) has been used to study the delayed, nonenzymatic lipid peroxidation (LP) initiated in rat liver microsomes by ferrous chloride. Following Fe2+ addition, the CL technique revealed a burst of light emission (peak, Phase II) which was preceded by a period of little or no detectable photon production (delay, Phase I) and succeeded by an increased emission (Phase III). Analysis of TBAR indicated a low rate of LP during the delay which increased more than fivefold during a 1-min period and which corresponded to the CL peak. The delay length depended on both the Fe2+ concentration and the microsome concentration; increased Fe2+ yielded longer delays while increased microsome concentration decreased the delay. As reported by others [J. R. Bucher, M. Tien, and S. D. Aust (1983) Biochem. Biophys. Res. Commun. 111, 777-784; J. M. Braughler, L. A. Duncan, and R. L. Chase (1986) J. Biol. Chem. 261, 10282-10289], Fe3+ also decreased the delay. The ferric-nitrilotriacetate (Fe3+-NTA) complex was found to be more efficient than "free" Fe3+ [Fe(NO3)3]; a 100 microM concentration of the 1:1 Fe3+-NTA complex eliminated the delay due to 100 microM Fe2+, whereas 400 microM Fe(NO3)3 reduced the delay from 17.5 to 2.5 min. Incubation under reduced O2 tension demonstrated a requirement for O2 during the delay. The use of antioxidants [butylated hydroxytoluene, (+)-catechin, promethazine, and uric acid] and inhibitors of the Haber-Weiss reaction (mannitol, Tris buffer, dimethyl sulfoxide, catalase, and superoxide dismutase) indicated that the initiating species has characteristics of a weak oxidizing radical capable of either hydrogen or electron abstraction from suitable target molecules. We hypothesize that the delay that is sensitive to the Fe2+:microsome ratio is due to reductive elimination of the initiating species by "free" Fe2+. The nature of the initiating species has yet to be determined; however, the argument is presented that the perferryl ion (Fe3+-O2-.) may possess the characteristics required for the initiator.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0003-9861
pubmed:author
pubmed:issnType
Print
pubmed:volume
259
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
372-81
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Delayed, ferrous iron-dependent peroxidation of rat liver microsomes.
pubmed:affiliation
Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't