The DOI matches its Crossref record; 68 of the 70 references it cites were found in a registry or an index.
An embryoprotective role for glucose‐6‐phosphate dehydrogenase in developmental oxidative stress and chemical teratogenesis
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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“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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Role of oxidative stress in female reproduction
Agarwal, A., Gupta, S., & Sharma, R. K. (2005) · Reproductive Biology and Endocrinology · doi:10.1186/1477-7827-3-28 · Cited by 1,729
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Onset of Maternal Arterial Blood Flow and Placental Oxidative Stress
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Metadata
- 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.
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2000-01
- Volume
- 14
- Issue
- 1
- Pages
- 111-127
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- 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
- 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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