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Title: Influence of zinc nutriture on expression of fetal alcohol syndrome in rat model

Journal Article · · Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)
OSTI ID:7024996

Excess EtOH intake during human pregnancy can be teratogenic, causing Fetal Alcohol Syndrome (FAS). Altered mineral metabolism may be one mechanism underlying development of FAS. The authors have examined the role of Zn nutriture in the teratogenicity of EtOH in Sprague-Dawley rats. Females (120-140 g) were fed isocaloric Lieber-DeCarli diets containing Zn at concentrations of 2 ..mu..g/ml (low;LZn), 30 ..mu..g/ml (adequate), or 300 ..mu..g/ml (supplemented); EtOH contributed either 0% of kcals (OEtOH) or 36% (EtOH). After 4 weeks females were bred and fed the same diets. Restricted fed groups were included to control for caloric intake. On d 21, rats were killed fetuses and placentas removed. Food intake was not affected by EtOH but decreased by 20% in LZn rats on d 19 and 20. EtOH and Zn intake influenced fetal size; most affected were LZnEtOH fetuses which weighed 12% less than controls. LZn groups had soft tissue and skeletal abnormalities, with the highest incidence in LZnEtOH fetuses. These effects were not noted in fetuses from restricted dams. Supplemental Zn did not prevent the teratogenic effects of EtOH possibly due to induced Cu deficiency as suggested by tissue Cu analyses. These data indicate that low maternal Zn intake may exacerbate the effects of EtOH, but excess Zn can also be deleterious.

Research Organization:
Univ. of California, Davis
OSTI ID:
7024996
Report Number(s):
CONF-8604222-
Journal Information:
Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States), Vol. 45:4; 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