Cited by 180Neonatal Health and BiochemistryRedox biology and oxidative stressPharmacological Effects and Toxicity Studies

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An embryoprotective role for glucose‐6‐phosphate dehydrogenase in developmental oxidative stress and chemical teratogenesis

NICOL, CHRISTOPHER J., ZIELENSKI, JULIAN, TSUI, LAP‐CHEE, WELLS, PETER G.·2000·The FASEB Journal

DOI 10.1096/fasebj.14.1.111

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Abstract

The primary recognized health risk from common deficiencies in glucose‐6‐phosphate dehydrogenase (G6PD), a cytoprotective enzyme for oxidative stress, is red blood cell hemolysis. Here we show that litters from untreated pregnant mutant mice with a hereditary G6PD deficiency had increased prenatal (fetal resorptions) and postnatal death. When treated with the anticonvulsant drug phenytoin, a human teratogen that is commonly used in pregnant women and causes embryonic oxidative stress, G6PD‐deficient dams had higher embryonic DNA oxidation and more fetal death and birth defects. The reported G6PD gene mutation was confirmed and used to genotype fetal resorptions, which were primarily G6PD deficient. This is the first evidence that G6PD is a developmentally critical cytoprotective enzyme for both endogenous and xenobiotic‐initiated embryopathic oxidative stress and DNA damage. G6PD deficiencies accordingly may have a broader biological relevance as important determinants of infertility, in utero and postnatal death, and teratogenesis.—Nicol, C. J., Zielenski, J., Tsui, L.‐C., Wells, P. G. An embryoprotective role for glucose‐6‐phosphate dehydrogenase in developmental oxidative stress and chemical teratogenesis. FASEB J. 14, 111–127(2000)

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Authors: NICOL, C. J., ZIELENSKI, J., TSUI, L., & WELLS, P. G.
Affiliations: University of Toronto (CA)
Hospital for Sick Children (CA)
Corresponding author: WELLS, PETER G.
ORCID: NICOL, CHRISTOPHER J.
WELLS, PETER G.
Venue: The FASEB Journal
Publisher: Wiley
Published: 2000-01
Volume: 14
Issue: 1
Pages: 111-127
ISSN: 0892-6638 (ISSN-L)
1530-6860
DOI: 10.1096/fasebj.14.1.111
OpenAlex: W1535461485
Cited by: 180
References: 70
Citations by year: 2026: 3 · 2025: 3 · 2024: 4 · 2023: 3 · 2022: 3 · 2021: 2 · 2020: 4 · 2019: 12 · 2018: 9 · 2017: 7 · 2016: 6 · 2015: 5 · 2014: 6 · 2013: 7 · 2012: 8
FWCI: 7.24
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: The FASEB Journal (publishedVersion)
PubMed (publishedVersion)
The HKU Scholars Hub (University of Hong Kong) (submittedVersion)
Funders: Society of Toxicology
Topics: Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal Health and Biochemistry
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Pharmacological Effects and Toxicity Studies
Keywords: glucose-6-phosphate dehydrogenase, glucose-6-phosphate dehydrogenase deficiency, phenytoin, fetal resorption, fetal death, congenital malformations, cytoprotection, pregnancy
MeSH terms: Animals, Base Sequence, DNA Damage, Embryo, Mammalian, Female, Embryonic and Fetal Development, Glucosephosphate Dehydrogenase, Heterozygote, Homozygote, Mice, Mutant Strains, Phenotype, Pregnancy, Teratogens, DNA Primers, Oxidative Stress, Mice

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An embryoprotective role for glucose‐6‐phosphate dehydrogenase in developmental oxidative stress and chemical teratogenesis

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