Mutagenicity, toxicity and repair of DNA base damage induced by oxidation

Bjelland, Svein; Seeberg, Erling

doi:10.1016/j.mrfmmm.2003.07.002

Cited by 445 publications

(355 citation statements)

References 396 publications

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“…Besides uracil, oxidation-damaged DNA bases are also substrates of UNG. UNG recognizes uracil derivatives in DNA generated from the oxidation of cytosine by hydroxyl radical attack or other oxidative processes [5,6]. Depletion or knockdown of UNG reduces cell proliferation, induces apoptosis, and increases cellular sensitivity to genotoxic stress [7,8].…”

Section: Introductionmentioning

confidence: 99%

Hydrogen peroxide mediated mitochondrial UNG1-PRDX3 interaction and UNG1 degradation

Liu

Gong

et al. 2016

Free Radical Biology and Medicine

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Section: Introductionmentioning

confidence: 99%

Hydrogen peroxide mediated mitochondrial UNG1-PRDX3 interaction and UNG1 degradation

Liu

Gong

et al. 2016

Free Radical Biology and Medicine

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“…Recent reviews on the mechanisms of oxidative DNA damage and repair have focussed on prevention and repair (Cooke et al, 2003), biochemical features , substrate specificities for glycosylases (Dizdaroglu, 2003), biological consequences (Wallace, 2002: Bjelland andSeeberg, 2003) and the role of iron (Kruszewski, 2003).…”

mentioning

confidence: 99%

Several pathways of hydrogen peroxide action that damage the E. coli genome

Asad

Almeida

et al. 2004

Genet. Mol. Biol.

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Hydrogen peroxide is an important reactive oxygen species (ROS) that arises either during the aerobic respiration process or as a by-product of water radiolysis after exposure to ionizing radiation. The reaction of hydrogen peroxide with transition metals imposes on cells an oxidative stress condition that can result in damage to cell components such as proteins, lipids and principally to DNA, leading to mutagenesis and cell death. Escherichia coli cells are able to deal with these adverse events via DNA repair mechanisms, which enable them to recover their genome integrity. These include base excision repair (BER), nucleotide excision repair (NER) and recombinational repair. Other important defense mechanisms present in Escherichia coli are OxyR and SosRS anti-oxidant inducible pathways, which are elicited by cells to avoid the introduction of oxidative lesions by hydrogen peroxide. This review summarizes the phenomena of lethal synergism between UV irradiation (254 nm) and H 2 O 2 , the cross-adaptive response between different classes of genotoxic agents and hydrogen peroxide, and the role of copper ions in the lethal response to H 2 O 2 under low-iron conditions. Key words: hydrogen peroxide, cross-adaptive response, lethal synergism, copper and iron. General AspectsThe appearance of aerobic forms of life was an important step in the evolutionary process, since oxygen consumption leads to the production of ten-fold more energy from glucose than does anaerobic metabolism (Meneghini, 1987). However, this process imposes constraints on cell viability, because of the generation of reactive oxygen species during respiration.The consecutive univalent reduction of molecular oxygen to water produces three active intermediates: superoxide anion (O 2 -• ), hydrogen peroxide (H 2 O 2 ) and hydroxyl radical (OH • ). These intermediates, collectively referred to as reactive oxygen species (ROS) are potent oxidants of lipids, proteins, and nucleic acids (Halliwell and Gutteridge, 1984;Mello-Filho and Meneghini, 1985;Meneghini, 1988). Among the oxidative DNA lesions, one of the major classes of DNA damage leads to modification in purine and pyrimidine bases, together with oligonucleotide strand breaks, DNA-protein cross-links and abasic sites. Increasing evidence suggests that the cumulative damage caused by ROS contributes to numerous degenerative diseases associated with aging, such as atherosclerosis, rheumatoid arthritis and cancer (Ames et al., 1993;Halliwell and Gutteridge, 1999).Living organisms have developed specific mechanisms to prevent the production and effects of ROS. The reduction of O 2 by cytochrome oxidase without yielding ROS, the superoxide dismutase catalysis of O 2 -• into H 2 O 2 through a dismutation reaction, the decomposition of H 2 O 2 by catalase and peroxidases, and the scavenging of ROS by some vitamins comprise part of the set of cellular antioxidant defenses (Halliwell and Gutteridge, 1999). Synthesis of the enzymes that catalyze these reactions is a part of the adaptive response tr...

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“…Other studies have also shown that smoking increases oxidative stress, resulting in genotoxicity, [6][7][8] which may affect cell replication and transcription and cause cell death and/or cell mutations.…”

Section: Discussionmentioning

confidence: 99%

Associação entre funções da via auditiva eferente e genotoxicidade em adultos jovens

Fronza¹,

Barreto²,

Tochetto³

et al. 2011

Braz. j. otorhinolaryngol. (Impr.)

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Ef ferent auditory pathways modulate outer hair cells of the cochlea, protect against noise, and improve the detection of sound sources in noisy environments. Genotoxicity is DNA damage. Aim:To study the association between auditory pathway efferent functions with genotoxic markers. The study also considered smoking and gender as two main variables. Methods:A prospective-clinical, quantitative, cross-sectional, contemporary study. The function of efferent auditory pathways and genotoxicity tests in 60 healthy young subjects were assessed. Results:The mean age of subjects was 24.86 years +/-3.68 years; there were 30 males and 30 females, 15 of each gender smokers and 15 non-smokers. Male smokers had a higher incidence of DPOEA suppression effect at 2000 and 6000 Hz in the left ear; female smokers had a higher prevalence of complaints of difficulty to hear in noisy environments; smokers and women had a higher mean DNA damage; subjects with complaints of hearing loss and tinnitus had higher genotoxicity. Conclusions:In young normal-hearing adults that complain about efferent auditory pathways functions, such as tinnitus and hearing impairment, there are possible associations with genotoxicity; interactions between gender and smoking are considered.

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Mutagenicity, toxicity and repair of DNA base damage induced by oxidation

Cited by 445 publications

References 396 publications

Hydrogen peroxide mediated mitochondrial UNG1-PRDX3 interaction and UNG1 degradation

Hydrogen peroxide mediated mitochondrial UNG1-PRDX3 interaction and UNG1 degradation

Several pathways of hydrogen peroxide action that damage the E. coli genome

Associação entre funções da via auditiva eferente e genotoxicidade em adultos jovens

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