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

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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Crossref · 10.1096/fasebj.14.1.111

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  • In animals with genetically impaired antioxidant enzyme activity and in diabetic rats with increased ROS levels, offspring have congenital abnormalities.

    “Burton (2009) reported that in animals with genetically impaired antioxidant enzyme activity and in diabetic rats in whom ROS levels were increased, the offspring had congenital abnormalities (Hagay et al. 1995;Eriksson, 1999;Nicol et al. 2000).”

    From Iron, Oxidative Stress and Health (2012) · cites this paper as Nicol et al. 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
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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