Does measurement of oxidative damage to DNA have clinical significance?

Cooke, Marcus S.; Oliński, Ryszard; Evans, Mark D.

doi:10.1016/j.cca.2005.09.009

Cited by 204 publications

(150 citation statements)

References 133 publications

Supporting

Mentioning

144

Contrasting

Unclassified

Order By: Relevance

“…Therefore, besides efficacy in correcting iron deficiency, one of the main criteria for selecting an iron supplementation protocol is that the supplemental iron should produce minimal toxicity. The oxidatively damaged DNA exacerbated by iron may be involved in the development of various pathological conditions (for review see 25,49). Considering the striking differences in the hepatic non-heme iron content found in piglets from the three experimental groups, 8-oxodG was used as a biomarker of iron-induced oxidative stress in piglet livers.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Benefits and Risks of Iron Supplementation in Anemic Neonatal Pigs

Lipiński¹,

Starzyński²,

Canonne‐Hergaux³

et al. 2010

The American Journal of Pathology

120

View full text Add to dashboard Cite

Iron deficiency is a common health problem. The most severe consequence of this disorder is iron deficiency anemia (IDA), which is considered the most common nutritional deficiency worldwide. Newborn piglets are an ideal model to explore the multifaceted etiology of IDA in mammals, as IDA is the most prevalent deficiency disorder throughout the early postnatal period in this species and frequently develops into a critical illness. Here, we report the very low expression of duodenal iron transporters in pigs during the first days of life. We postulate that this low expression level is why the iron demands of the piglet body are not met by iron absorption during this period. Interestingly, we found that a low level of duodenal divalent metal transporter 1 and ferroportin, two iron transporters located on the apical and basolateral membrane of duodenal absorptive enterocytes, respectively, correlates with abnormally high expression of hepcidin, despite the poor hepatic and overall iron status of these animals. Parenteral iron supplementation by a unique intramuscular administration of large amounts of iron dextran is current practice for the treatment of IDA in piglets. However, the potential toxicity of such supplemental iron implies the necessity for caution when applying this treatment. Here we demonstrate that a modified strategy for iron supplementation of newborn piglets with iron dextran improves the piglets' hematological status, attenuates the induction of hepcidin expression, and minimizes the toxicity of the administered iron. (Am J Pathol

show abstract

Section: Discussionmentioning

confidence: 99%

“…The base modification 8-oxodG is regarded as a good biomarker of oxidatively damaged DNA (for review see 25). The hepatic level of this oxidative DNA adduct was analyzed in piglets receiving supplemental iron and control animals.…”

Section: Hepatic Level Of 8-oxodg Is Increased In Fedex Supplemented mentioning

confidence: 99%

Benefits and Risks of Iron Supplementation in Anemic Neonatal Pigs

Lipiński¹,

Starzyński²,

Canonne‐Hergaux³

et al. 2010

The American Journal of Pathology

120

View full text Add to dashboard Cite

show abstract

“…Although more than 20 different types of oxidatively altered purine and pyrimidine bases have been detected in nucleic acids [144][145][146][147], guanine is the most reactive of the nucleic acid bases [148]. Therefore, the oxidized base 8OHG is the most abundant among the oxidized bases [138].…”

Section: Rna Oxidation and Repairmentioning

confidence: 99%

Nucleic acid oxidation in Alzheimer disease

Moreira

Nunomura

Nakamura

et al. 2008

Free Radical Biology and Medicine

186

112

View full text Add to dashboard Cite

Increasing evidence suggests that oxidative stress is intimately associated with Alzheimer disease pathophysiology. Nucleic acids (nuclear DNA, mitochondrial DNA, and RNA) are one of the several cellular macromolecules damaged by reactive oxygen species, particularly the hydroxyl radical. Because neurons are irreplaceable and survive as long as the organism does, they need elaborate defense mechanisms to ensure their longevity. In Alzheimer disease, however, an accumulation of nucleic acid oxidation is observed, indicating an increased level of oxidative stress and/or a decreased capacity to repair the nucleic acid damage. In this review, we present data supporting the notion that mitochondrial and metal abnormalities are key sources of oxidative stress in Alzheimer disease. Furthermore, we outline the mechanisms of nucleic acid oxidation and repair. Finally, evidence showing the occurrence of nucleic acid oxidation in Alzheimer disease will be discussed.

show abstract

“…To this end, we were motivated to develop a sensitive, robust and general approach to quantify DNA lesions caused by the known classes of inflammation chemistry shown in Figure 2. It should be noted that there are many different products of DNA oxidation and alkylation arising from exposure to ionizing radiation and other insults, [18][19][20][21][22][23][24] but these species are not unlikely to form under the biological conditions of inflammation. 4 Further, we have recently initiated efforts to include the cytosine and guanine halo-adducts arising from reactions of DNA with neutrophil-derived HOCl.…”

Section: Introductionmentioning

confidence: 99%

Quantification of DNA damage products resulting from deamination, oxidation and reaction with products of lipid peroxidation by liquid chromatography isotope dilution tandem mass spectrometry

et al. 2008

View full text Add to dashboard Cite

The analysis of damage products as biomarkers of inflammation has been hampered by a poor understanding of the chemical biology of inflammation, the lack of sensitive analytical methods, and a focus on single chemicals as surrogates for inflammation. To overcome these problems, we developed a general and sensitive liquid chromatographic tandem mass spectrometry (LC/MS-MS) method to quantify, in a single DNA sample, the nucleoside forms of seven DNA lesions reflecting the range of chemistries associated with inflammation: 2′-deoxyuridine, 2′-deoxyxanthosine, and 2′-deoxyinosine from nitrosative deamination; 8-oxo-2′-deoxyguanosine from oxidation; and 1,N 2 -etheno-2′-deoxyguanosine, 1,N 6 -etheno-2′-deoxyadenosine, and 3,N 4 -etheno-2′-deoxycytidine arising from reaction of DNA with lipid peroxidation products. Using DNA purified from cells or tissues under conditions that minimize artifacts, individual nucleosides are purified by HPLC and quantified by isotope-dilution, electrospray ionization LC/MS-MS. The method can be applied to other DNA damage products and requires 4-6 days to complete depending upon the number of samples. Search terms

show abstract

Does measurement of oxidative damage to DNA have clinical significance?

Cited by 204 publications

References 133 publications

Benefits and Risks of Iron Supplementation in Anemic Neonatal Pigs

Benefits and Risks of Iron Supplementation in Anemic Neonatal Pigs

Nucleic acid oxidation in Alzheimer disease

Quantification of DNA damage products resulting from deamination, oxidation and reaction with products of lipid peroxidation by liquid chromatography isotope dilution tandem mass spectrometry

Contact Info

Product

Resources

About