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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-4-19
pubmed:abstractText
The mechanism of arsine (AsH3) induced hemolysis was studied in vitro using isolated red blood cells (RBCs) from the rat or dog. AsH3-induced hemolysis of dog red blood cells was completely blocked by carbon monoxide (CO) preincubation and was reduced by pure oxygen (O2) compared to incubations in air. Since CO and O2 bind to heme and also reduce hemolysis, these results suggested a reaction between AsH3 and hemoglobin in the heme-ligand binding pocket or with the heme iron. Further, sodium nitrite induction of methemoglobin (metHb) to 85% and 34% of total Hb in otherwise intact RBCs resulted in 56% and 16% decreases in hemolysis, respectively, after incubation for 4 h. This provided additional evidence for the involvement of hemoglobin in the AsH3-induced hemolysis mechanism. Reactions between AsH3 and hemoglobin were studied in solutions of purified dog hemoglobin. Spectrophotometric studies of the reaction of AsH3 with various purified hemoglobin species revealed that AsH3 reacted with HbO2 to produce metHb and, eventually, degraded Hb characterized by gross precipitation of the protein. AsH3 did not alter the spectrum of deoxyHb and did not cause degradation of metHb in oxygen, but bound to and reduced metHb in the absence of oxygen. These data indicate that a reaction of AsH3 with oxygenated hemoglobin HbO2, may lead to hemolysis, but there are reactions between AsH3 and metHb that may not be directly involved in the hemolytic process.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0098-4108
pubmed:author
pubmed:issnType
Print
pubmed:day
9
pubmed:volume
47
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
145-57
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Reactions of arsine with hemoglobin.
pubmed:affiliation
Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, USA.
pubmed:publicationType
Journal Article