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PubMed1994

Effect of pre-treatment with aspirin on alcohol-induced neural tube defects in the TO mouse fetuses.

This study was planned to investigate the effects of ethanol on the genetic susceptibility of the TO mouse to neural tube malformations and to determine the ameliorative effects, if any, of aspirin a potent prostaglandin inhibitor. The TO mouse exhibits a spontaneous incidence of 3.6% exencephaly. The mice were exposed to single (i.p.) dose of 0.03 ml/gm body weight of a solution of (25%v/v) of absolute alcohol in physiological saline on day 7 or 8 of gestation. Subteratogenic doses (150 or 200 mg/kg) of aspirin were administered (i.p.) an hour before ethanol exposure. Fetuses were collected on day 18 and compared with those of the untreated, and saline treated pair-fed pair-watered controls as well as with those of the aspirin alone treatment group. A total of 175 litters were studied. Alcohol caused a three-fold increase against the background incidence of exencephaly. Several craniofacial anomalies and growth retardation were also observed. Alizarin red-S stained skeletal preparations revealed extensive malformations of the craniofacial skeleton in the exencephalic fetuses. Both doses of aspirin administered prior to alcohol treatment significantly accentuated the alcohol-induced prenatal mortality. The rescue effect of aspirin on alcohol-induced intrauterine growth retardation was also significant although fetal weight was not restored to levels comparable to those of the controls. Pre-treatment with aspirin (both 150 and 200 mg/kg) on day 8 of gestation resulted in a numerical, though not statistically significant increase in alcohol-induced exencephaly. On the other hand pre-administration of the lower dose on day 7 exencephaly. On the other hand pre-administration of the lower dose on day 7 of gestation caused a significant reduction while the higher dose gave rise to a significant increase in the incidence of this malformation. Aspirin also reduced the frequency of alcohol-induced arched palate and the baseline exencephaly. These data provide evidence for the possible interaction of alcohol with the genetic susceptibility to exencephaly in this strain of mice. The lack of a clear dose-dependent antagonistic effect of aspirin on alcohol-induced exencephaly suggests that the production of this malformation is probably not mediated by prostaglandin as it was shown for limb and renal abnormalities (Randall, C.L., Anton, R.F. and Becker, H.C. (1991). Aspirin dose dependently reduces alcohol induced birth defects and prostaglandin E levels in mice. Teratology 44, 521-529).

Anencephaly↗
PubMed1988

Interaction between the splotch mutation and retinoic acid in mouse neural tube defects in vitro.

The interaction between the splotch gene (Sp) and all-trans retinoic acid (RA) was investigated using cytogenetically marked Sp/+ and +/+ mouse embryos cultured in the presence of RA. Retinoic acid retarded the development of and had a teratogenic effect on mouse embryos in culture. In particular, RA had seemingly opposite effects on the posterior neural tube, inducing abnormally early fusion in some embryos and causing a dose-dependent delay in others. When the effects of RA on identified Sp/+ and +/+ embryos were compared, the only observed difference in their responses was in the degree of the delay in posterior neuropore (PNP) closure. At the end of the culture period, among the untreated control embryos, the Sp heterozygotes showed retardation of PNP closure compared to +/+ embryos. In addition, the RA treatment was found to have induced a greater delay in posterior neural tube closure in Sp/+ than in +/+ embryos. The basis for this difference in response to RA is presumed to be the retardation of PNP closure that is caused by the Sp gene in heterozygous form. The effects of the gene and the teratogen are additive and the gene carriers thus have greater mean PNP lengths at the end of culture. Since the length of the PNP is an indication of an embryo's likelihood of developing spina bifida, this provides an explanation for the observation that Sp/+ embryos are more sensitive to the spina bifida-causing effects of RA than are +/+ embryos.

Animals↗