Journal ArticleDOI
Accumulation of 8-oxoguanine in the cellular DNA and the alteration of the OGG1 expression during ischemia-reperfusion injury in the rat kidney.
Kazuhiko Tsuruya,Masato Furuichi,Yohei Tominaga,Michiya Shinozaki,Masanori Tokumoto,Takahiro Yoshimitsu,Kyoichi Fukuda,Hidetoshi Kanai,Hideki Hirakata,Mitsuo Iida,Yusaku Nakabeppu +10 more
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TLDR
The accumulation of 8-oxo-dG in the mitochondrial DNA rather than in nuclear DNA is likely to be involved in the pathogenic responses such as necrosis of renal tubular cells during I/R injury of the kidney, together with an altered level of OGG1 expression.About:
This article is published in DNA Repair.The article was published on 2003-02-03. It has received 88 citations till now. The article focuses on the topics: Kidney metabolism & In situ hybridization.read more
Citations
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Journal ArticleDOI
Two distinct pathways of cell death triggered by oxidative damage to nuclear and mitochondrial DNAs
TL;DR: Both cell deaths were triggered by single‐strand breaks (SSBs) that had accumulated in the respective DNAs, and were suppressed by knockdown of adenine DNA glycosylase encoded by MutY homolog, thus indicating that excision ofAdenine opposite 8‐oxoG lead to the accumulation of SSBs in each type of DNA.
Journal ArticleDOI
Acetylation of human 8-oxoguanine-DNA glycosylase by p300 and its role in 8-oxoguanine repair in vivo.
TL;DR: It is shown that O GG1 is acetylated by p300 in vivo predominantly at Lys338/Lys341, and a novel regulatory function of OGG1 acetylation in repair of its substrates in oxidatively stressed cells is proposed.
Journal ArticleDOI
High urea and NaCl carbonylate proteins in renal cells in culture and in vivo, and high urea causes 8-oxoguanine lesions in their DNA
TL;DR: Oxidative stress, associated with high urea, causes 8-oxoguanine DNA lesions in mIMCD3 cell DNA and carbonylation increases over the uremic range of urea concentration, indicating that urea can contribute directly to thecarbonylation found in uremia.
Journal ArticleDOI
Oxidative DNA damage and obesity in type 2 diabetes mellitus
TL;DR: The results indicate that serum 8-OHdG is increased already in prediabetes suggesting oxidative DNA damage to be present with minor elevation of blood glucose levels (BGLs) and obesity has an additive effect to increased BGL contributing to oxidativeDNA damage.
Journal ArticleDOI
8-oxoguanine causes spontaneous de novo germline mutations in mice
Mizuki Ohno,Kunihiko Sakumi,Ryutaro Fukumura,Masato Furuichi,Yuki Iwasaki,Masaaki Hokama,Toshimichi Ikemura,Teruhisa Tsuzuki,Yoichi Gondo,Yusaku Nakabeppu +9 more
TL;DR: It is shown here that endogenous 8-oxoG caused de novo spontaneous and heritable G to T mutations in mice, which occurred at different stages in the germ cell lineage and were distributed throughout the chromosomes.
References
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Journal ArticleDOI
Oxidants, antioxidants, and the degenerative diseases of aging
TL;DR: It is argued that this damage to DNA, protein, and lipid is a major contributor to aging and to degenerative diseases of aging such as cancer, cardiovascular disease, immune-system decline, brain dysfunction, and cataracts.
Journal ArticleDOI
Oxygen-derived free radicals in postischemic tissue injury.
TL;DR: It is now clear that oxygen-derived free radicals play an important part in several models of experimentally induced reperfusion injury, and Dysfunction induced by free radicals may be a major component of ischemic diseases of the heart, bowel, liver, kidney, and brain.
Book
DNA Repair and Mutagenesis
TL;DR: Nucleotide excision repair in mammalian cells: genes and proteins Mismatch repair The SOS response and recombinational repair in prokaryotes Mutagenesis in proKaryote Mutagenisation in eukaryotes Other DNA damage tolerance responses in eUKaryotes.
Journal ArticleDOI
A model for p53-induced apoptosis
Kornelia Polyak,Kornelia Polyak,Yong Xia,Jay L. Zweier,Kenneth W. Kinzler,Bert Vogelstein,Bert Vogelstein +6 more
TL;DR: Examination of transcripts induced by p53 expression before the onset of apoptosis stimulated additional biochemical and pharmacological experiments suggesting that p53 results in apoptosis through a three-step process: the transcriptional induction of redox-related genes; the formation of reactive oxygen species; and the oxidative degradation of mitochondrial components, culminating in cell death.
Journal ArticleDOI
Oxidative damage and mitochondrial decay in aging
TL;DR: Evidence supports the suggestion that age-associated accumulation of mitochondrial deficits due to oxidative damage is likely to be a major contributor to cellular, tissue, and organismal aging.
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