Abstract
Excessive ethanol intake during pregnancy can cause birth defects in humans and is referred to as fetal alcohol syndrome (FAS). Because of the characteristic changes that are similar in FAS and zinc (Zn) deficiency, we have examined the role of Zn nutriture in the teratogenicity of ethanol in Sprague-Dawley rats. Female Sprague-Dawley rats were adapted to liquid diets containing Zn at 2 μg/ml (LZn), 30 μg/ml (AZn), or 300 μg/ml (HZn); ethanol contributed either 0% or 36% of kilocalories. Ethanol consumption resulted in reduced fetal growth and retarded skeletal development. Ethanol had no effect on whole body fetal Zn concentrations; however, copper (CU) deficiency was induced in the HZn fetuses. Ethanol consumption resulted in higher than normal fetal liver CuZnSOD activity in the LZn and AZn groups. Fetuses from HZn dams showed no ethanol effect on CuZnSOD activity, suggesting that the low availability of Cu to the fetus prevented the increase in CuZnSOD activity in response to ethanol. The increase in the activity of fetal CuZnSOD in LZn and AZn groups is consistent with the concept that the metabolism of ethanol results in free radical generation in fetal tissue. Because excessive free radical levels may result in tissue damage, this may be one mechanism contributing to the expression of FAS.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 257-274 |
| Number of pages | 18 |
| Journal | Drug-Nutrient Interactions |
| Volume | 5 |
| Issue number | 4 |
| State | Published - 1988 |
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ASJC Scopus subject areas
- Medicine(all)
- Pharmacology
Cite this
Altered mineral metabolism : A mechanism underlying the fetal alcohol syndrome in rats. / Zidenberg-Cherr, S.; Benak, P. A.; Hurley, L. S.; Keen, Carl L.
In: Drug-Nutrient Interactions, Vol. 5, No. 4, 1988, p. 257-274.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Altered mineral metabolism
T2 - A mechanism underlying the fetal alcohol syndrome in rats
AU - Zidenberg-Cherr, S.
AU - Benak, P. A.
AU - Hurley, L. S.
AU - Keen, Carl L
PY - 1988
Y1 - 1988
N2 - Excessive ethanol intake during pregnancy can cause birth defects in humans and is referred to as fetal alcohol syndrome (FAS). Because of the characteristic changes that are similar in FAS and zinc (Zn) deficiency, we have examined the role of Zn nutriture in the teratogenicity of ethanol in Sprague-Dawley rats. Female Sprague-Dawley rats were adapted to liquid diets containing Zn at 2 μg/ml (LZn), 30 μg/ml (AZn), or 300 μg/ml (HZn); ethanol contributed either 0% or 36% of kilocalories. Ethanol consumption resulted in reduced fetal growth and retarded skeletal development. Ethanol had no effect on whole body fetal Zn concentrations; however, copper (CU) deficiency was induced in the HZn fetuses. Ethanol consumption resulted in higher than normal fetal liver CuZnSOD activity in the LZn and AZn groups. Fetuses from HZn dams showed no ethanol effect on CuZnSOD activity, suggesting that the low availability of Cu to the fetus prevented the increase in CuZnSOD activity in response to ethanol. The increase in the activity of fetal CuZnSOD in LZn and AZn groups is consistent with the concept that the metabolism of ethanol results in free radical generation in fetal tissue. Because excessive free radical levels may result in tissue damage, this may be one mechanism contributing to the expression of FAS.
AB - Excessive ethanol intake during pregnancy can cause birth defects in humans and is referred to as fetal alcohol syndrome (FAS). Because of the characteristic changes that are similar in FAS and zinc (Zn) deficiency, we have examined the role of Zn nutriture in the teratogenicity of ethanol in Sprague-Dawley rats. Female Sprague-Dawley rats were adapted to liquid diets containing Zn at 2 μg/ml (LZn), 30 μg/ml (AZn), or 300 μg/ml (HZn); ethanol contributed either 0% or 36% of kilocalories. Ethanol consumption resulted in reduced fetal growth and retarded skeletal development. Ethanol had no effect on whole body fetal Zn concentrations; however, copper (CU) deficiency was induced in the HZn fetuses. Ethanol consumption resulted in higher than normal fetal liver CuZnSOD activity in the LZn and AZn groups. Fetuses from HZn dams showed no ethanol effect on CuZnSOD activity, suggesting that the low availability of Cu to the fetus prevented the increase in CuZnSOD activity in response to ethanol. The increase in the activity of fetal CuZnSOD in LZn and AZn groups is consistent with the concept that the metabolism of ethanol results in free radical generation in fetal tissue. Because excessive free radical levels may result in tissue damage, this may be one mechanism contributing to the expression of FAS.
UR - http://www.scopus.com/inward/record.url?scp=0024212175&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0024212175&partnerID=8YFLogxK
M3 - Article
C2 - 3240709
AN - SCOPUS:0024212175
VL - 5
SP - 257
EP - 274
JO - Drug-Nutrient Interactions
JF - Drug-Nutrient Interactions
SN - 0272-3530
IS - 4
ER -