Pregnancy outcome in ethanol-treated mice with folic acid supplementation in saccharose

Yanaguita, Maira Yuli; Gutierrez, Cristiane Minot; Ribeiro, C. N. M.; Lima, Guilherme Alves; Machado, Hélio Rubens; Peres, Luíz César

doi:10.1007/s00381-007-0427-1

Cited by 18 publications

(20 citation statements)

References 28 publications

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“…This may result in too few cells for fusion of the neural folds (Copp et al, 2003; Greene and Kopp, 2006). Animal models also suggest that alcohol exposure may play an indirect role in NTD development (Yanaguita et al, 2008) by contributing to folic acid deficiency via increased excretion of folic acid by the kidneys (McMartin, 1984; Muldoon and McMartin, 1994). …”

Section: Discussionmentioning

confidence: 99%

“…Alcohol is a known teratogen, with effects that may be more pronounced during organogenesis (Yanaguita et al, 2008). A potential association between alcohol consumption and NTDs was first described in a case series more than 25 years ago (Friedman, 1982); however, the biological mechanisms by which alcohol impacts neural tube development are not well understood.…”

Section: Introductionmentioning

confidence: 99%

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Periconceptional maternal alcohol consumption and neural tube defects

Makelarski

Romitti

Sun

et al. 2013

Birth Defects Research

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BACKGROUND Neural tube defects (NTD)s, which occur when the neural tube fails to close during early gestation, are some of the most common birth defects worldwide. Alcohol is a known teratogen and has been shown to induce NTDs in animal studies, although most human studies have failed to corroborate these results. Using data from the National Birth Defects Prevention Study, associations between maternal reports of periconceptional (1 month prior through 2 months postconception) alcohol consumption and NTDs were examined. METHODS NTD cases and unaffected live born control infants, delivered from 1997 through 2005, were included. Interview reports of alcohol consumption (quantity, frequency, variability, and type) were obtained from 1223 case mothers and 6807 control mothers. Adjusted odds ratios (aOR)s and 95% confidence intervals were estimated using multivariable logistic regression analysis. RESULTS For all NTDs combined, most aORs for any alcohol consumption, one or more binge episodes, and different type(s) of alcohol consumed were near unity or modestly reduced (≥0.7

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Periconceptional maternal alcohol consumption and neural tube defects

Makelarski

Romitti

Sun

et al. 2013

Birth Defects Research

View full text Add to dashboard Cite

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“…However, with a folate free diet, a low ethanol dose was as deleterious as a high dose. Yanaguita et al (2008) concluded that supplementation with the recommended dose of folic acid (2 mg/kg), was not effective in preventing the deleterious teratogenic effects induced by ethanol, indicating the need for an increased dose. Firat et al (2005) in their experiment on rats, administered Retinoic acid in different doses, orally on GD8.…”

Section: Discussionmentioning

confidence: 99%

“…Folic acid has been shown to reduce the incidence of neural tube defects caused by valproic acid (Dawson et al, 2006;Padmanabhan and Shafiullah, 2003) retinoic acid (Reynolds et al, 2003;Firat et al, 2005), ochratoxin A (Katagiri et al 2007), Fumonisin B1 (Sadler et al, 2002), ethanol (Yanaguita et al, 2008), arsenic (Gefrides et al, 2002) and hyperthermia (Shin and Shiota, 1999;Li et al, 2003). Its role in the prevention of other congenital defects has not yet been fully explored.…”

Section: Discussionmentioning

confidence: 99%

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Role of folic acid in chlorpyrifos induced teratogenicity in mice

Tafweez¹

2014

Afr. J. Biotechnol.

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Folic acid is known to reduce the incidence of neural tube defects, in animal experiments however, it has not been effective in reducing the congenital anomalies caused by antiepileptics and many other chemicals. Pesticides of organophosphate group such as chlorpyrifos are widely used in agriculture and household, and are shown to be teratogenic in animal studies. This study was designed to explore the effect of folic acid on chlorpyrifos induced teratogenicity. Pregnant mice were divided into groups of 8 animals each, and were exposed to oral dose of chlorpyrifos and/or folic acid on gestation days (GD) 6 and 7 or GD 1 to 15. Fetuses were recovered on 15 th day of gestation. On morphological and morphometeric examination it was found that chlorpyrifos is teratogenic to mice fetuses in an oral dose of 100 ug/gbw when given on GD 6 and 7. It was embryo toxic and caused growth retardation and morphological anomalies of skull, body curvature, skin, limbs, eyes and ears. Folic acid in a dose of 2 ug/gbw, when given at the time of chlorpyrifos exposure (GD 6 and 7), lead to significant improvement in crown-rump (CR) length and weight of fetuses, reduction in the number of resorptions and frequency of anomalies. However the CR length and weight of fetuses given folic acid and chlorpyrifos were significantly less than the control. There was no additional benefit of giving folic acid in the same dose from GD1 to 15. Thus this study was aimed at confirming the teratogenic potential of cholorpyrifos in mice and assessing the role of folic acid in the prevention of teratogenesis induced by chlorpyrifos.

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Genetic Factors Contributing to FASD

Chudley

2010

Fetal Alcohol Spectrum Disorder

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Pregnancy outcome in ethanol-treated mice with folic acid supplementation in saccharose

Abstract: The study demonstrated that dietary supplementation with folate in saccharose is an accessible means of consumption that could be further diffused but in an increased dose than recommended to reduce the teratogenic effects of ethanol.

Cited by 18 publications

References 28 publications

Periconceptional maternal alcohol consumption and neural tube defects

Periconceptional maternal alcohol consumption and neural tube defects

Role of folic acid in chlorpyrifos induced teratogenicity in mice

Genetic Factors Contributing to FASD

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