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ToxSci Advance Access published online on May 26, 2006
Toxicological Sciences, doi:10.1093/toxsci/kfl024
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© The Author 2006. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received March 25, 2006
Accepted May 16, 2006

Genetic Toxicology

Ethanol-induced Fetal Dysmorphogenesis in the Mouse is Diminished by High Anti-oxidative Capacity of the Mother

Parri Wentzel 1 * and Ulf J. Eriksson 1

1 Department of Medical Cell Biology, Uppsala Universitet, Biomedical Center, P.O. Box 571, SE-751 23 Uppsala, Sweden

* To whom correspondence should be addressed.
Parri Wentzel, E-mail: Parri.Wentzel{at}medcellbiol.uu.se


  Abstract

Intrauterine exposure to ethanol causes embryonic and fetal maldevelopment. Oxidative stress in mother and offspring has been suggested to be part of the teratogenic mechanism of ethanol. Here we aimed to assess the importance of maternal and fetal antioxidative capability for the risk of dysmorphogenesis in the offspring. We used male and female mice with different levels of superoxide dismutase (SOD) activity - wild type (WT), mice with a targeted SOD mutation (KO, decreased CuZn SOD mRNA), and mice transgenic for SOD (TG, increased CuZn SOD mRNA). Female WT, KO (heterozygous) and TG (heterozygous) mice were given drinking water containing 20% ethanol before and throughout gestation. Non-ethanol-exposed WT, KO and TG mice served as controls. The female mice were mated with males with identical genotype and the pregnancy was interrupted on gestational day 18 when the offspring was evaluated and genotyped. Fetal hepatic isoprostane (8-epi-PGF2{alpha}) levels were measured to assess the degree of fetal oxidative stress.

Exposure to 20% ethanol decreased fetal weight by 9-13% in the three groups. Ethanol exposure roughly doubled the rates of maldeveloped WT and KO offspring, but did not affect TG offspring. The fetal hepatic levels of 8-epi-PGF2{alpha} were increased in the ethanol-exposed WT and KO mice, but not in ethanol-exposed TG mice. Ethanol exposure preferentially damaged WT fetuses in pregnant KO mice, whereas no such effect was found in the litters of ethanol-consuming TG mice.

Administration of ethanol to pregnant mice disturbs embryogenesis by oxidative stress, and the adverse effects are more pronounced in offspring of mice with low anti-oxidative capacity.

Keywords: ethanol; mouse; transgene; targeted mutation; oxygen radical(s); iso-prostane(s); 8-epi-PGF2{alpha}.
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