Cockayne Syndrome B Protects Against Methamphetamine-Enhanced Oxidative DNA Damage in Murine Fetal Brain and Postnatal Neurodevelopmental Deficits
| Autor: | Peter G. Wells, Andrea W. Wong, Gordon P. McCallum |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
musculoskeletal diseases
Male congenital hereditary and neonatal diseases and abnormalities medicine.medical_specialty Guanine Physiology DNA repair DNA damage Clinical Biochemistry Motor Activity Biology medicine.disease_cause Biochemistry Methamphetamine Lesion Mice chemistry.chemical_compound Pregnancy Internal medicine medicine Animals heterocyclic compounds Poly-ADP-Ribose Binding Proteins Molecular Biology General Environmental Science Mice Knockout Genetics nutritional and metabolic diseases Brain Cell Biology Meth Motor coordination Oxidative Stress Original Research Communications DNA Repair Enzymes Endocrinology Liver chemistry In utero General Earth and Planetary Sciences Central Nervous System Stimulants Female medicine.symptom Oxidative stress DNA Damage medicine.drug |
| Zdroj: | Antioxidants & Redox Signaling. 14:747-756 |
| ISSN: | 1557-7716 1523-0864 |
| DOI: | 10.1089/ars.2009.2946 |
| Popis: | Methamphetamine (METH) increases the oxidative DNA lesion 8-oxoguanine (8-oxoG) in fetal mouse brain, and causes postnatal motor coordination deficits after in utero exposure. Like oxoguanine glycosylase 1 (OGG1), the Cockayne syndrome B (CSB) protein is involved in the repair of oxidatively damaged DNA, although its function is unclear. Here we used CSB-deficient Csbm/m knockout mice to investigate the developmental role of DNA oxidation and CSB in METH-initiated neurodevelopmental deficits. METH (40 mg/kg intraperitoneally) administration to pregnant Csb females on gestational day 17 increased 8-oxoG levels in Csbm/m fetal brains (p |
| Databáze: | OpenAIRE |
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