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Mechanism of guanine-specific DNA damage by oxidative stress and its role in carcinogenesis and aging.
The mechanism of sequence-specific DNA damage in relation to carcinogenesis and aging is discussed and the sequence specificity of DNA damage is presumably determined by redox potential of reactive species; ionization potential of DNA bases; and site-specific binding of metal ion to DNA. Expand
Mechanism of Telomere Shortening by Oxidative Stress
It is concluded that the formation of 8‐oxodG at the GGG triplet in telomere sequence induced by oxidative stress could participate in acceleration of telomeres shortening. Expand
Site‐specific DNA damage at GGG sequence by oxidative stress may accelerate telomere shortening
It is concluded that the site‐specific DNA damage at the GGG sequence by oxidative stress may play an important role in increasing the rate of telomere shortening with aging. Expand
Oxidative and nitrative DNA damage in animals and patients with inflammatory diseases in relation to inflammation-related carcinogenesis
It is proposed that 8-nitroguanine is a promising biomarker to evaluate the potential risk of inflammation-mediated carcinogenesis and excessive amounts of reactive nitrogen species produced via iNOS during chronic inflammation may play a key role in carcinogenesis by causing DNA damage. Expand
Oxidative Stress and Its Significant Roles in Neurodegenerative Diseases and Cancer
Reactive oxygen and nitrogen species have been implicated in diverse pathophysiological conditions, including inflammation, neurodegenerative diseases and cancer. Accumulating evidence indicates thatExpand
Requirement of glutathione and cysteine in guanine-specific oxidation of DNA by carcinogenic potassium bromate.
It is speculated that reduction of KBrO3 by SH compounds in renal proximal tubular cells yields bromine oxides andbromine radicals, which are the reactive species that cause guanine oxidation, leading to renal carcinogenesis of K BrO3. Expand
Mechanism of DNA damage induced by bromate differs from general types of oxidative stress.
A representative reactive oxygen species (ROS), hydroxyl radical (*OH), is a highly reactive species and induces DNA backbone breakage. *OH also oxidizes every DNA base. The interaction of *OH withExpand
Mechanism of DNA cleavage induced by sodium chromate(VI) in the presence of hydrogen peroxide.
Results indicate that sodium chromate(VI) reacts with hydrogen peroxide to form tetraperoxochromate(V), leading to the production of the hydroxyl radical, which causes every base alteration and deoxyribose-phosphate backbone breakage. Expand
Mechanism of apoptosis induced by doxorubicin through the generation of hydrogen peroxide.
The mechanism of apoptosis induced by DOX in the human leukemia cell line HL-60 and the H(2)O(2)-resistant sub-clone, HP100 was investigated, suggesting that the critical apoptotic trigger of DOX is considered to be oxidative DNA damage by the DOX-induced direct H( 2)O (2) generation, although DOx-induced apoptosis may involve topoisomerase II inhibition. Expand
Oxidative DNA Damage by Vitamin A and Its Derivative via Superoxide Generation*
It is reported here that vitamin A (retinol) and its derivative (retinal) caused cellular DNA cleavage detected by pulsed field gel electrophoresis, suggesting the involvement of H2O2 in cellular DNA damage. Expand