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Title: Hepatic copper content in normal and toxic milk neonatal mice

Conference · · Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)
OSTI ID:5461746

Adult toxic milk mice exhibit over ten times normal amounts of hepatic copper. Patterns of hepatic copper accumulation were followed in neonates born both to normal (+/-/+/-, +/-/tx/-) and mutant (tx/-/tx/-) mothers. At birth all offspring of normal dams have high hepatic copper levels which then decline over the next two weeks; after this time levels in normal neonates continue to decline while in mutant neonates levels rise sharply, both genotypes attaining adult levels by six weeks. Conversely, all offspring of mutant females are born severely copper deficient, a condition exacerbated by ingestion of the copper deficient milk that these females produce, which leads to death during the second week. Such infants can be rescued if fostered to normal lactating females at birth; copper levels rise for two weeks and then fall in normal infants but continue to rise in mutant infants. Beginning at the third postnatal week then, hepatic copper levels are attributable to infant genotype, while prior to this time concentrations reflect maternal genotype. The pattern of uptake of /sup 67/Cu by neonates is consistent with the copper content observed above. Those hepatic cuproproteins which vary according to genotype also indicate that the third week is the time when infant genotype becomes expressed in phenotype. The significant accumulation of copper in the livers of fetuses carried by normal dams is compared to that occurring in the livers of suckling mutants.

Research Organization:
Univ. of Massachusetts, Amherst
OSTI ID:
5461746
Report Number(s):
CONF-8604222-; TRN: 86-028422
Journal Information:
Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States), Vol. 45:3; Conference: 70. annual meeting of the Federation of American Society for Experimental Biology, St. Louis, MO, USA, 13 Apr 1986
Country of Publication:
United States
Language:
English