Postnatal closure of membranous ventricular septal defects in Sprague‐Dawley rat pups after maternal exposure with trimethadione

Fleeman, T.L.; Cappon, Gregg D.; Hurtt, Mark E.

doi:10.1002/bdrb.20011

Cited by 26 publications

(44 citation statements)

References 11 publications

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“…Although 70% of small VSDs in human infants usually resolve on their own during the first 2 years of life, large VSDs are known to cause failure to thrive, especially if compounded by other anomalies (Turner et al, 2002;Rudolph, 2009). Similarly, in rodents, small VSDs can resolve whereas the closure of larger VSDs may be less common (Fleeman et al, 2004). It would be of interest to conduct a study in our mouse model postnatally to determine whether the VSD or the thinner ventricular walls are present at birth or whether they can resolve prenatally or in the early postnatal period.…”

Section: Discussionmentioning

confidence: 99%

Moderately high intake of folic acid has a negative impact on mouse embryonic development

Mikael

Deng

Paul

et al. 2012

Birth Defects Research

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BACKGROUND:The incidence of neural tube defects has diminished considerably since the implementation of food fortification with folic acid (FA). However, the impact of excess FA intake, particularly during pregnancy, requires investigation. In a recent study, we reported that a diet supplemented with 20-fold higher FA than the recommended intake for rodents had adverse effects on embryonic mouse development at embryonic days (E)10.5 and 14.5. In this report, we examined developmental outcomes in E14.5 embryos after administering a diet supplemented with 10-fold higher FA than recommended to pregnant mice with and without a mild deficiency of methylenetetrahydrofolate reductase (MTHFR). METHODS: Pregnant mice with or without a deficiency in MTHFR were fed a control diet (recommended FA intake of 2 mg/kg diet for rodents) or an FA-supplemented diet (FASD; 10-fold higher than the recommended intake [20 mg/kg diet]). At E14.5, mice were examined for embryonic loss and growth retardation, and hearts were assessed for defects and for ventricular wall thickness. RESULTS: Maternal FA supplementation was associated with embryonic loss, embryonic delays, a higher incidence of ventricular septal defects, and thinner left and right ventricular walls, compared to mothers fed control diet. CONCLUSIONS: Our work suggests that even moderately high levels of FA supplementation may adversely affect fetal mouse development. Additional studies are warranted to evaluate the impact of high folate intake in pregnant women. Birth Defects Research (Part A) 97:47À52,

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Section: Discussionmentioning

confidence: 99%

Moderately high intake of folic acid has a negative impact on mouse embryonic development

Mikael

Deng

Paul

et al. 2012

Birth Defects Research

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“…6). The mean incidence of VSD in control was 14 AE 25% and entirely attributable to one litter with a 44% incidence of VSD (normal background rates are 2-3%; Fleeman et al, 2004;Solomon et al, 1997). No DMO was detected in the serum of this dam, ruling out the possibility that these spurious findings were the result of dosing error and therefore there was no rationale for excluding this dam from study.…”

Section: The Effect Of Dmo On Malformationsmentioning

confidence: 94%

“…However, more recent studies reported dose-limiting maternal toxicity above 300 mg/kg b.i.d. and only a 50% incidence of VSD (Fleeman et al, 2004). We believe the heightened maternal sensitivity to TMD was the result of the re-derivation of the Sprague-Dawley rat by Charles River in 1998 to yield the Crl:CD(SD)IGS BR foundation colony (White and Lee, 1998).…”

Section: Introductionmentioning

confidence: 99%

“…We believe the heightened maternal sensitivity to TMD was the result of the re-derivation of the Sprague-Dawley rat by Charles River in 1998 to yield the Crl:CD(SD)IGS BR foundation colony (White and Lee, 1998). Reduced maternal tolerance resulted in lower embryonic exposures, which may explain the disparity of the incidences of VSD between by Fleeman et al (2004) and by Solomon et al (1997) and Veuthey, 1990. A further, possibly related, contributing factor may have been genetic drift in the Ndemethylation activities of the pre-and post-rederived SpragueDawley rat.…”

Section: Introductionmentioning

confidence: 99%

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Maternal rat serum concentrations of dimethadione do not explain intra-litter differences in the incidence of dimethadione-induced birth defects, including novel findings in foetal lung

et al. 2014

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“…On the other hand, it has been proved that small VSDs induced by prenatal exposure to trimethadione did not significantly affect fetal viability or growth (7). Unlike all other COX inhibitor studies, the developmental effect was treatment-related.…”

Section: Discussionmentioning

confidence: 94%

Congenital ventricular septal defects and prenatal exposure to cyclooxygenase inhibitors

Burdan

Szumiło

Dudka

et al. 2006

Braz J Med Biol Res

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Ventricular septal defects (VSDs) are common congenital abnormalities which have been reported to be associated with maternal fever and various environmental factors. The aim of the present study was to evaluate the effect of prenatal exposure to cyclooxygenase (COX) inhibitors on heart defects. A retrospective statistical analysis was performed using data collected in our laboratory during various teratological studies carried out on albino CRL:(WI)WUBR Wistar strain rats from 1997 to 2004. The observations were compared with concurrent and historic control data, as well as findings from other developmental toxicological studies with selective and nonselective COX-2 inhibitors. Despite the lack of significant differences in the frequency of VSDs between drug-exposed and control groups, statistical analysis by the two-sided Mantel-Haenszel test and historical control data showed a higher incidence of heart defects in offspring exposed to nonselective COX inhibitors (30.06/10,000). Unlike other specific inhibitors, aspirin (46.26/10,000) and ibuprofen (106.95/ 10,000) significantly increased the incidence of the VSD when compared with various control groups (5. 38-19.72/10,000). No significant differences in length or weight were detected between fetuses exposed to COX inhibitors and born with VSD and non-malformed offsprings. However, a statistically significant increase of fetal body length and decrease of body mass index were found in fetuses exposed to COX inhibitors when compared with untreated control. We conclude that prenatal exposure to COX inhibitors, especially aspirin and ibuprofen, increased the incidence of VSDs in rat offspring but was not related to fetal growth retardation.

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Postnatal closure of membranous ventricular septal defects in Sprague‐Dawley rat pups after maternal exposure with trimethadione

Cited by 26 publications

References 11 publications

Moderately high intake of folic acid has a negative impact on mouse embryonic development

Moderately high intake of folic acid has a negative impact on mouse embryonic development

Maternal rat serum concentrations of dimethadione do not explain intra-litter differences in the incidence of dimethadione-induced birth defects, including novel findings in foetal lung

Congenital ventricular septal defects and prenatal exposure to cyclooxygenase inhibitors

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