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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1976-8-23
pubmed:abstractText
Daily administration of increasing doses intraperitoneally of 2.5-4.0 mg NaCN/kg to male Wistar rats for 5 weeks produced acute signs of poisoning immediately post-injection but no sign of chronic toxicity except lower final body weights than in control rats. CN-treated rats had less liver copper than controls, but not below the range of normality, and their liver mitochondrial membranes were 24% less able to bind adenine nucleotides than control membranes. No other biochemical or pathological sign of copper deficiency occurred. Liver cytochrome oxidase activity was normal after the 5 weeks of CN-administration, as was the ability of liver mitochondria to synthesize phospholipids. The ultrastructure of hepatocytes was normal without evidence of the enlarged, misshapen mitochondria produced by copper deficiency. Normal cytochrome oxidase activity of liver mitochondria, together with reduced liver copper levels and reduced binding affinity of mitochondrial membranes for adenine nucleotides, indicate that the membrane binding site for adenine nucleotides is not cytochrome oxidase per se but may involve copper, perhaps by virtue of its cationicity. With repeated exposure to CN- rats develop tolerance to acute poisoning. It is suggested that this may be due to the switch in glucose catabolism towards the pentose pathway at the expense of other pathways.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0004-945X
pubmed:author
pubmed:issnType
Print
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
343-8
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1976
pubmed:articleTitle
Coppr deficiency in the rat. Relationship to chronic cyanide poisoning.
pubmed:publicationType
Journal Article