ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Oxoguanine glycosylase 1 protects against methamphetamine-enhanced fetal brain oxidative DNA damage and neurodevelopmental deficits.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 95 citations in OpenAlex.
- Maternal, healthcare, and nutritional factors influencing birth defects in China from 2019 to 2025: a systematic review and meta-analysis.Frontiers in pediatrics · 2026Review
- Impact of Prenatal Alcohol Exposure on the Cerebral Circulation: Potential Implications for Stroke.Advances in experimental medicine and biology · 2026Review
- Exploring the epigenetic landscape: The role of 5-hydroxymethylcytosine in neurodevelopmental disorders.Cambridge prisms. Precision medicine · 2024Review
- Methamphetamine exposure drives cell cycle exit and aberrant differentiation in rat hippocampal-derived neurospheres.Frontiers in pharmacology · 2023Article
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- Daily, limited access to methamphetamine self-administration during pregnancy leads to increased methamphetamine sensitivity in adult offspring.Developmental psychobiology · 2023Article
- MTH1 and OGG1 maintain a low level of 8-oxoguanine in Alzheimer's brain, and prevent the progression of Alzheimer's pathogenesis.Scientific reports · 2021Article
- The Adverse Effects of Prenatal METH Exposure on the Offspring: A Review.Frontiers in pharmacology · 2021Review
- DNA damage and synaptic and behavioural disorders in glucose-6-phosphate dehydrogenase-deficient mice.Redox biology · 2020Article
- Murine Models for the Study of Fetal Alcohol Spectrum Disorders: An Overview.Frontiers in pediatrics · 2020Review
- Critical Role of Oxidatively Damaged DNA in Selective Noradrenergic Vulnerability.Neuroscience · 2019Article
- Prenatal Exposure to Methamphetamine: Up-Regulation of Brain Receptor Genes.Frontiers in neuroscience · 2019Article
- The roles of base excision repair enzyme OGG1 in gene expression.Cellular and molecular life sciences : CMLS · 2018Review
- Article
- Breast cancer 1 (BRCA1)-deficient embryos develop normally but are more susceptible to ethanol-initiated DNA damage and embryopathies.Redox biology · 2016Article
- Effect of 8-oxoguanine glycosylase deficiency on aflatoxin B1 tumourigenicity in mice.Mutagenesis · 2015Article
- Interactions of HIV and drugs of abuse: the importance of glia, neural progenitors, and host genetic factors.International review of neurobiology · 2014Review
- Article
- Brain glucose-6-phosphate dehydrogenase protects against endogenous oxidative DNA damage and neurodegeneration in aged mice.ACS chemical neuroscience · 2013Article
- Congenital abnormality effect of methamphetamine on histological, cellular and chromosomal defects in fetal mice.Iranian journal of reproductive medicine · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In utero methamphetamine (METH) exposure enhances the oxidative DNA lesion 7,8-dihydro-8-oxoguanine (8-oxoG) in CD-1 fetal mouse brain, and causes long-term postnatal motor coordination deficits. Herein we used oxoguanine glycosylase 1 (ogg1) knock-out mice to determine the pathogenic roles of 8-oxoG and OGG1, which repairs 8-oxoG, in METH-initiated neurodevelopmental anomalies. Administration of METH (20 or 40 mg/kg) on gestational day 17 to pregnant +/- OGG1-deficient females caused a drug dose- and gene dose-dependent increase in 8-oxoG levels in OGG1-deficient fetal brains (p < 0.05). Female ogg1 knock-out offspring exposed in utero to high-dose METH exhibited gene dose-dependent enhanced motor coordination deficits for at least 12 weeks postnatally (p < 0.05). Contrary to METH-treated adult mice, METH-exposed CD-1 fetal brains did not exhibit altered apoptosis or DNA synthesis, and OGG1-deficient offspring exposed in utero to METH did not exhibit postnatal dopaminergic nerve terminal degeneration, suggesting different mechanisms. Enhanced 8-oxoG repair activity in fetal relative to adult organs suggests an important developmental protective role of OGG1 against in utero genotoxic stress. These observations provide the most direct evidence to date that 8-oxoG constitutes an embryopathic molecular lesion, and that functional fetal DNA repair protects against METH teratogenicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.