Monoclonal Antibody to Single-Stranded DNA: A Potential Tool for DNA Repair Studies

Cooke, Marcus S.; Patel, Kalpana; Ahmad, Jabeen; Holloway, Karen; Evans, Mark D.; Lunec, Joseph

doi:10.1006/bbrc.2001.4954

Cited by 28 publications

(12 citation statements)

References 37 publications

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“…Potentially these oligomers could undergo intra/extracellular 5′‐3′ exonucleolytic digestion to ultimately produce lesion‐containing oligomers 6–7 nucleotides long (51, 57). This type of postexcision processing has not been demonstrated for 8‐OH‐dG‐containing oligomers, although there is some tantalizing evidence that 8‐OH‐dG‐containing oligomers may be present in urine, but whether these are reflective of NER is open to debate (58, 59).…”

Section: Prevention Of Lesion Persistance: Dna Repairmentioning

confidence: 99%

Oxidative DNA damage: mechanisms, mutation, and disease

et al. 2003

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Oxidative DNA damage is an inevitable consequence of cellular metabolism, with a propensity for increased levels following toxic insult. Although more than 20 base lesions have been identified, only a fraction of these have received appreciable study, most notably 8-oxo-2'deoxyguanosine. This lesion has been the focus of intense research interest and been ascribed much importance, largely to the detriment of other lesions. The present work reviews the basis for the biological significance of oxidative DNA damage, drawing attention to the multiplicity of proteins with repair activities along with a number of poorly considered effects of damage. Given the plethora of (often contradictory) reports describing pathological conditions in which levels of oxidative DNA damage have been measured, this review critically addresses the extent to which the in vitro significance of such damage has relevance for the pathogenesis of disease. It is suggested that some shortcomings associated with biomarkers, along with gaps in our knowledge, may be responsible for the failure to produce consistent and definitive results when applied to understanding the role of DNA damage in disease, highlighting the need for further studies.

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Section: Prevention Of Lesion Persistance: Dna Repairmentioning

confidence: 99%

Oxidative DNA damage: mechanisms, mutation, and disease

et al. 2003

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“…However, it should be remembered that the products of NER and MTH1 both require further processing to result in 8-oxodG. Moreover, there is little evidence that 8-oxodG is a product of DNA repair itself [13]. Oxidatively damaged DNA bases are mostly repaired by the base excision repair pathway (BER), although some components of the nucleotide excision repair pathway may also play a role in the repair of some oxidized bases in DNA [14,15].…”

Section: Introductionmentioning

confidence: 99%

Urinary excretion rates of 8-oxoGua and 8-oxodG and antioxidant vitamins level as a measure of oxidative status in healthy, full-term newborns

Dziaman¹,

Gackowski²,

Różalski³

et al. 2007

Free Radical Research

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The aim of the present study was to evaluate the oxidative status in healthy full-term children and piglets. Urinary excretion of 8-oxoGua (8-oxoguanine) and 8-oxodG (8-oxo-2'-deoxyguanosine) were determined using HPLC/GS/MS methodology and concentrations of vitamins A, C and E with HPLC technique. The levels of 8-oxoGua in urine samples were about 7-8 times higher in newborn children and piglets when compared with the level of adult subjects, while in the case of 8-oxodG the difference was about 2.5 times. The levels of vitamin C and E in umbilical cord blood of newborn children significantly depend on the concentration of these compounds in their mother's blood. However, the values of vitamin C in human's cord blood were about 2-times higher than in respective mother blood, while the level of vitamin E showed an opposite trend. The results suggest that: (i) healthy, full-term newborns are under potential oxidative stress; (ii) urinary excretion of 8-oxoGua and 8-oxodG may be a good marker of oxidative stress in newborns; and (iii) antioxidant vitamins, especially vitamin C, play an important role in protecting newborns against oxidative stress.

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“…Inactivation of enzymes like DNA, RNA polymerases leads to the impairment in the metabolism of nucleic acids due to single and double strand breaks. [30] It is also presumed that an enhanced damage to membrane as well as to DNA is associated with a decline in the production of adenosine triphosphate.…”

Section: Discussionmentioning

confidence: 99%