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Embryo transfers between C57BL/6J and DBA/2J mice: Examination of a maternal effect on ethanol teratogenesis.

Gilliam D - Front Genet (2014)

Bottom Line: We hypothesized that, following maternal alcohol exposure, B6 and D2 fetuses gestating within B6 mothers, as compared to D2 mothers, will exhibit a higher frequency of malformations.This suggests the D2 maternal uterine environment did not offer any protection against ethanol teratogenesis for B6 fetuses.No definitive conclusions can be drawn because too few viable D2 litters were produced.

View Article: PubMed Central - PubMed

Affiliation: School of Psychological Sciences, University of Northern Colorado Greeley, CO, USA.

ABSTRACT
Genetic factors influence fetal alcohol spectrum disorders (FASDs) in both humans and animals. Experiments using inbred and selectively bred mouse stocks that controlled for (1) ethanol dose, (2) maternal and fetal blood ethanol levels, and (3) fetal developmental exposure stage, show genotype can affect teratogenic outcome. Other experiments distinguish the teratogenic effects mediated by maternal genotype from those mediated by fetal genotype. One technique to distinguish maternal versus fetal genotype effect is to utilize embryo transfers. This study is the first to examine ethanol teratogenesis - fetal weight deficits and mortality, and digit, kidney, and vertebral malformations - in C57BL/6J (B6) and DBA/2J (D2) fetuses that were transferred as blastocysts into B6 and D2 dams. We hypothesized that, following maternal alcohol exposure, B6 and D2 fetuses gestating within B6 mothers, as compared to D2 mothers, will exhibit a higher frequency of malformations. On day 9 of pregnancy, females were intubated (IG) with either 5.8 g/kg ethanol (E) or maltose-dextrin (MD). Other females were mated within strain and treated with either ethanol or maltose, or were not exposed to either treatment. Implantation rates were affected by genotype. Results show more B6 embryos implanted into D2 females than B6 females (p < 0.05; 47% vs. 23%, respectively). There was no difference in the percentage of D2 embryos implanting into B6 and D2 females (14 and 16%, respectfully). Litter mortality averaged 24% across all experimental groups. Overall, in utero ethanol exposure reduced mean litter weight compared to maltose treatment (E = 1.01 g; MD = 1.19 g; p < 0.05); but maltose exposed litters with transferred embryos weighed more than similarly treated natural litters (1.30 g vs. 1.11 g; p < 0.05). Approximately 50% of all ethanol exposed B6 fetuses exhibited some malformation (digit, vertebral, and/or kidney) regardless of whether they were transferred into a B6 or D2 female, or were naturally conceived. This suggests the D2 maternal uterine environment did not offer any protection against ethanol teratogenesis for B6 fetuses. One of the questions remaining is the how the B6 uterine environment affects D2 teratogenesis. No definitive conclusions can be drawn because too few viable D2 litters were produced.

No MeSH data available.


Related in: MedlinePlus

Fetal weight (grams) was similarly affected by ethanol treatment in both transferred and naturally conceived fetuses (p > 0.05), while maltose-exposed fetuses resulting from embryo transfers weighed more than similarly treated naturally conceived fetuses (p < 0.05).
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Figure 1: Fetal weight (grams) was similarly affected by ethanol treatment in both transferred and naturally conceived fetuses (p > 0.05), while maltose-exposed fetuses resulting from embryo transfers weighed more than similarly treated naturally conceived fetuses (p < 0.05).

Mentions: Analysis of mean litter weight showed a main effect of treatment [ethanol < maltose; F(2,42) = 4.58, p < 0.05] and an interaction between pregnancy type (transferred vs. natural) and treatment [ethanol vs. maltose; F(1,42) = 4.48, p < 0.05]. Litter weight for both transferred and natural litters was similarly decreased by ethanol exposure. In contrast, maltose exposed litters with transferred embryos weighed more than similarly treated natural litters (p < 0.05; Figure 1).


Embryo transfers between C57BL/6J and DBA/2J mice: Examination of a maternal effect on ethanol teratogenesis.

Gilliam D - Front Genet (2014)

Fetal weight (grams) was similarly affected by ethanol treatment in both transferred and naturally conceived fetuses (p > 0.05), while maltose-exposed fetuses resulting from embryo transfers weighed more than similarly treated naturally conceived fetuses (p < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4263196&req=5

Figure 1: Fetal weight (grams) was similarly affected by ethanol treatment in both transferred and naturally conceived fetuses (p > 0.05), while maltose-exposed fetuses resulting from embryo transfers weighed more than similarly treated naturally conceived fetuses (p < 0.05).
Mentions: Analysis of mean litter weight showed a main effect of treatment [ethanol < maltose; F(2,42) = 4.58, p < 0.05] and an interaction between pregnancy type (transferred vs. natural) and treatment [ethanol vs. maltose; F(1,42) = 4.48, p < 0.05]. Litter weight for both transferred and natural litters was similarly decreased by ethanol exposure. In contrast, maltose exposed litters with transferred embryos weighed more than similarly treated natural litters (p < 0.05; Figure 1).

Bottom Line: We hypothesized that, following maternal alcohol exposure, B6 and D2 fetuses gestating within B6 mothers, as compared to D2 mothers, will exhibit a higher frequency of malformations.This suggests the D2 maternal uterine environment did not offer any protection against ethanol teratogenesis for B6 fetuses.No definitive conclusions can be drawn because too few viable D2 litters were produced.

View Article: PubMed Central - PubMed

Affiliation: School of Psychological Sciences, University of Northern Colorado Greeley, CO, USA.

ABSTRACT
Genetic factors influence fetal alcohol spectrum disorders (FASDs) in both humans and animals. Experiments using inbred and selectively bred mouse stocks that controlled for (1) ethanol dose, (2) maternal and fetal blood ethanol levels, and (3) fetal developmental exposure stage, show genotype can affect teratogenic outcome. Other experiments distinguish the teratogenic effects mediated by maternal genotype from those mediated by fetal genotype. One technique to distinguish maternal versus fetal genotype effect is to utilize embryo transfers. This study is the first to examine ethanol teratogenesis - fetal weight deficits and mortality, and digit, kidney, and vertebral malformations - in C57BL/6J (B6) and DBA/2J (D2) fetuses that were transferred as blastocysts into B6 and D2 dams. We hypothesized that, following maternal alcohol exposure, B6 and D2 fetuses gestating within B6 mothers, as compared to D2 mothers, will exhibit a higher frequency of malformations. On day 9 of pregnancy, females were intubated (IG) with either 5.8 g/kg ethanol (E) or maltose-dextrin (MD). Other females were mated within strain and treated with either ethanol or maltose, or were not exposed to either treatment. Implantation rates were affected by genotype. Results show more B6 embryos implanted into D2 females than B6 females (p < 0.05; 47% vs. 23%, respectively). There was no difference in the percentage of D2 embryos implanting into B6 and D2 females (14 and 16%, respectfully). Litter mortality averaged 24% across all experimental groups. Overall, in utero ethanol exposure reduced mean litter weight compared to maltose treatment (E = 1.01 g; MD = 1.19 g; p < 0.05); but maltose exposed litters with transferred embryos weighed more than similarly treated natural litters (1.30 g vs. 1.11 g; p < 0.05). Approximately 50% of all ethanol exposed B6 fetuses exhibited some malformation (digit, vertebral, and/or kidney) regardless of whether they were transferred into a B6 or D2 female, or were naturally conceived. This suggests the D2 maternal uterine environment did not offer any protection against ethanol teratogenesis for B6 fetuses. One of the questions remaining is the how the B6 uterine environment affects D2 teratogenesis. No definitive conclusions can be drawn because too few viable D2 litters were produced.

No MeSH data available.


Related in: MedlinePlus