دورية أكاديمية
أعرض في EDS

Oxidative stress increases M1dG, a major peroxidation-derived DNA adduct, in mitochondrial DNA.

التفاصيل البيبلوغرافية
العنوان: Oxidative stress increases M1dG, a major peroxidation-derived DNA adduct, in mitochondrial DNA.
المؤلفون: Wauchope OR; A.B. Hancock, Jr., Memorial Laboratory for Cancer Research, Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN, USA., Mitchener MM; Department of Chemistry, Vanderbilt University School of Medicine, Nashville, TN, USA., Beavers WN; Department of Chemistry, Vanderbilt University School of Medicine, Nashville, TN, USA., Galligan JJ; A.B. Hancock, Jr., Memorial Laboratory for Cancer Research, Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN, USA., Camarillo JM; A.B. Hancock, Jr., Memorial Laboratory for Cancer Research, Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN, USA., Sanders WD; A.B. Hancock, Jr., Memorial Laboratory for Cancer Research, Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN, USA., Kingsley PJ; A.B. Hancock, Jr., Memorial Laboratory for Cancer Research, Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN, USA., Shim HN; Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.; Department of Pharmacology, Vanderbilt Institute of Chemical Biology, Center in Molecular Toxicology, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN, USA., Blackwell T; Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.; Department of Pharmacology, Vanderbilt Institute of Chemical Biology, Center in Molecular Toxicology, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN, USA., Luong T; Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.; Department of Pharmacology, Vanderbilt Institute of Chemical Biology, Center in Molecular Toxicology, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN, USA., deCaestecker M; Departments of Cell and Developmental Biology, Surgery and Medicine, USA., Fessel JP; Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.; Department of Pharmacology, Vanderbilt Institute of Chemical Biology, Center in Molecular Toxicology, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN, USA., Marnett LJ; A.B. Hancock, Jr., Memorial Laboratory for Cancer Research, Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN, USA.; Department of Chemistry, Vanderbilt University School of Medicine, Nashville, TN, USA.; Department of Pharmacology, Vanderbilt Institute of Chemical Biology, Center in Molecular Toxicology, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN, USA.
المصدر: Nucleic acids research [Nucleic Acids Res] 2018 Apr 20; Vol. 46 (7), pp. 3458-3467.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Oxford University Press Country of Publication: England NLM ID: 0411011 Publication Model: Print Cited Medium: Internet ISSN: 1362-4962 (Electronic) Linking ISSN: 03051048 NLM ISO Abbreviation: Nucleic Acids Res Subsets: MEDLINE
أسماء مطبوعة: Publication: 1992- : Oxford : Oxford University Press
Original Publication: London, Information Retrieval ltd.
مواضيع طبية MeSH: DNA, Mitochondrial/*metabolism , Mitochondria/*genetics , Oxidative Stress/*genetics , Purine Nucleosides/*metabolism, Animals ; Bone Morphogenetic Protein Receptors, Type II/genetics ; DNA Adducts/genetics ; DNA Adducts/metabolism ; DNA, Mitochondrial/genetics ; Electron Transport/drug effects ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Gene Expression Regulation/genetics ; Humans ; Hypertension, Pulmonary/genetics ; Hypertension, Pulmonary/metabolism ; Hypertension, Pulmonary/pathology ; Lipid Peroxidation/genetics ; Mice ; Mice, Transgenic ; Mitochondria/pathology ; Mutagenesis/genetics ; Oxidants/pharmacology ; Purine Nucleosides/biosynthesis ; Reactive Oxygen Species/chemistry ; Superoxides/metabolism
مستخلص: Reactive oxygen species (ROS) are formed in mitochondria during electron transport and energy generation. Elevated levels of ROS lead to increased amounts of mitochondrial DNA (mtDNA) damage. We report that levels of M1dG, a major endogenous peroxidation-derived DNA adduct, are 50-100-fold higher in mtDNA than in nuclear DNA in several different human cell lines. Treatment of cells with agents that either increase or decrease mitochondrial superoxide levels leads to increased or decreased levels of M1dG in mtDNA, respectively. Sequence analysis of adducted mtDNA suggests that M1dG residues are randomly distributed throughout the mitochondrial genome. Basal levels of M1dG in mtDNA from pulmonary microvascular endothelial cells (PMVECs) from transgenic bone morphogenetic protein receptor 2 mutant mice (BMPR2R899X) (four adducts per 106 dG) are twice as high as adduct levels in wild-type cells. A similar increase was observed in mtDNA from heterozygous null (BMPR2+/-) compared to wild-type PMVECs. Pulmonary arterial hypertension is observed in the presence of BMPR2 signaling disruptions, which are also associated with mitochondrial dysfunction and oxidant injury to endothelial tissue. Persistence of M1dG adducts in mtDNA could have implications for mutagenesis and mitochondrial gene expression, thereby contributing to the role of mitochondrial dysfunction in diseases.
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معلومات مُعتمدة: K08 HL121174 United States HL NHLBI NIH HHS; R25 DK096999 United States DK NIDDK NIH HHS; T32 GM065086 United States GM NIGMS NIH HHS; S10 OD017997 United States OD NIH HHS; P01 CA077839 United States CA NCI NIH HHS; R01 CA087819 United States CA NCI NIH HHS; R25 GM062459 United States GM NIGMS NIH HHS
المشرفين على المادة: 0 (3-(2'-deoxy-beta-D-erythro-pentofuranosyl)pyrimido(1,2-alpha)purin-10(3H)-one)
0 (DNA Adducts)
0 (DNA, Mitochondrial)
0 (Oxidants)
0 (Purine Nucleosides)
0 (Reactive Oxygen Species)
11062-77-4 (Superoxides)
EC 2.7.11.30 (Bmpr2 protein, mouse)
EC 2.7.11.30 (Bone Morphogenetic Protein Receptors, Type II)
تواريخ الأحداث: Date Created: 20180214 Date Completed: 20190715 Latest Revision: 20240323
رمز التحديث: 20240323
مُعرف محوري في PubMed: PMC5909422
DOI: 10.1093/nar/gky089
PMID: 29438559
قاعدة البيانات: MEDLINE
الوصف
تدمد:1362-4962
DOI:10.1093/nar/gky089