Protective effect of folic acid against oxidative stress produced in 21-day postpartum rats by maternal-ethanol chronic consumption during pregnancy and lactation period

Cano, Mercedes; Ayala, Antonio; Murillo, María Luisa Ojeda; Carreras, Olimpia

doi:10.1080/10715760100300011

Cited by 79 publications

(59 citation statements)

References 42 publications

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“…The current study provides in vivo evidence for the antioxidative activity of folate and FDH. Our results also support the beneficial effects of folate supplementation to developing embryos, especially for those at risk of FAS (28,29). By overexpressing and knocking down fdh, we observed that the embryonic THF level was modulated by the FDH level.…”

Section: Discussionsupporting

confidence: 68%

Ethanol-Induced Upregulation of 10-Formyltetrahydrofolate Dehydrogenase Helps Relieve Ethanol-Induced Oxidative Stress

Hsiao

Lin

Chung

et al. 2014

Molecular and Cellular Biology

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Alcoholism induces folate deficiency and increases the risk for embryonic anomalies. However, the interplay between ethanol exposure and embryonic folate status remains unclear. To investigate how ethanol exposure affects embryonic folate status and one-carbon homeostasis, we incubated zebrafish embryos in ethanol and analyzed embryonic folate content and folate enzyme expression. Exposure to 2% ethanol did not change embryonic total folate content but increased the tetrahydrofolate level approximately 1.5-fold. The expression of 10-formyltetrahydrofolate dehydrogenase (FDH), a potential intracellular tetrahydrofolate reservoir, was increased in both mRNA and protein levels. Overexpressing recombinant FDH in embryos alleviated the ethanol-induced oxidative stress in ethanol-exposed embryos. Further characterization of the zebrafish fdh promoter revealed that the ؊124/؉40 promoter fragment was the minimal region required for transactivational activity. The results of site-directed mutagenesis and binding analysis revealed that Sp1 is involved in the basal level of expression of fdh but not in ethanol-induced upregulation of fdh. On the other hand, CEBP␣ was the protein that mediated the ethanol-induced upregulation of fdh, with an approximately 40-fold increase of fdh promoter activity when overexpressed in vitro. We concluded that upregulation of fdh involving CEBP␣ helps relieve embryonic oxidative stress induced by ethanol exposure.

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Section: Discussionsupporting

confidence: 68%

Ethanol-Induced Upregulation of 10-Formyltetrahydrofolate Dehydrogenase Helps Relieve Ethanol-Induced Oxidative Stress

Hsiao

Lin

Chung

et al. 2014

Molecular and Cellular Biology

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“…The exact mechanisms remain unknown, but the addition of the free radical scavenging enzyme superoxide dismutase has been shown to significantly reverse the effects of ethanol in vitro [Amini et al, 2009;Davis et al, 1990]. Using antioxidants, these anomalies have been partially reversed in vivo, implying that oxidative stress plays a partial role in their development [Cano et al, 2001;Peng et al, 2005;Reimers et al, 2006].…”

Section: Alcohol As a Teratogenmentioning

confidence: 99%

Screening, Diagnosing and Prevention of Fetal Alcohol Syndrome: Is This Syndrome Treatable

Ismail¹,

Buckley²,

Budacki³

et al. 2010

Dev Neurosci

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Prenatal alcohol exposure can lead to a wide range of adverse effects on a developing fetus. As a whole, these teratogenic outcomes are generally known as fetal alcohol spectrum disorders, the most severe of which is fetal alcohol syndrome (FAS). Clinically, children diagnosed with FAS vary greatly in their presentation of symptoms, likely due to the amount of alcohol and timing of exposure, as well as maternal and genetic influences. All these factors play a role in determining the mechanisms through which alcohol damages a developing brain, the details of which are still largely unknown. However, continuing research and recent developments have provided promising results that may lead to screening mechanisms and treatment therapies for children with FAS. Here we review the teratogenic effects of alcohol, strategies for detecting maternal alcohol consumption, identification of fetal biological markers, and prevention methods for FAS.

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“…This is in agreement with previous results indicating the anti-lipid peroxidation properties of folic acid. 18) Although 1 mM of THF acid only partially prevented the formation of LP, induction of oxidative damage to lipids was totally prevented by 25 mM THF.…”

Section: )mentioning

confidence: 99%

Comparative Study of thein VitroProtective Effects of Several Antioxidants on Elongation Factor 2 under Oxidative Stress Conditions

Argüelles

Cano

Machado

et al. 2010

Bioscience, Biotechnology, and Biochemistry

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Protective effect of folic acid against oxidative stress produced in 21-day postpartum rats by maternal-ethanol chronic consumption during pregnancy and lactation period

Cited by 79 publications

References 42 publications

Ethanol-Induced Upregulation of 10-Formyltetrahydrofolate Dehydrogenase Helps Relieve Ethanol-Induced Oxidative Stress

Ethanol-Induced Upregulation of 10-Formyltetrahydrofolate Dehydrogenase Helps Relieve Ethanol-Induced Oxidative Stress

Screening, Diagnosing and Prevention of Fetal Alcohol Syndrome: Is This Syndrome Treatable

Comparative Study of thein VitroProtective Effects of Several Antioxidants on Elongation Factor 2 under Oxidative Stress Conditions

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