Accumulation of oxidatively generated DNA damage in the brain: A mechanism of neurotoxicity
- 1 February 2007
- journal article
- Published by Elsevier in Free Radical Biology and Medicine
- Vol. 42 (3) , 385-393
Abstract
No abstract availableKeywords
This publication has 47 references indexed in Scilit:
- In vivo oxidative metabolism of a major peroxidation-derived DNA adduct, M 1 dGProceedings of the National Academy of Sciences, 2006
- Differential modulation of base excision repair activities during brain ontogeny: Implications for repair of transcribed DNAMechanisms of Ageing and Development, 2006
- Accumulation of lipid peroxidation-derived DNA lesions: Potential lead markers for chemoprevention of inflammation-driven malignanciesMutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 2005
- Neonatal alcohol exposure increases malondialdehyde (MDA) and glutathione (GSH) levels in the developing cerebellumDevelopmental Brain Research, 2005
- A rat model of smoke inhalation injury: Influence of combustion smoke on gene expression in the brainToxicology and Applied Pharmacology, 2005
- Chemical and Biological Evidence for Base Propenals as the Major Sourceof the Endogenous M1dG Adduct in CellularDNAJournal of Biological Chemistry, 2005
- Imbalanced Base Excision Repair in Response to Folate Deficiency Is Accelerated by Polymerase β HaploinsufficiencyJournal of Biological Chemistry, 2004
- Developmental changes in expression and subcellular localization of the DNA repair glycosylase, MYH, in the rat brainJournal of Neurochemistry, 2003
- An overview of the development, validation, and application of neurobehavioral and neuromolecular toxicity assessment batteries: potential applications to combustion toxicologyToxicology, 1996
- Overexpression of N-methylpurine-DNA glycosylase in Chinese hamster ovary cells renders them more sensitive to the production of chromosomal aberrations by methylating agents — a case of imbalanced DNA repairMutation Research/DNA Repair, 1995