Oxidative damage to DNA: Formation, measurement, and biological significance

Cadet, Jean; Berger, M.; Douki, Thierry; Ravanat, Jean‐Luc

doi:10.1007/3-540-61992-5_5

Cited by 267 publications

(314 citation statements)

References 381 publications

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“…A more detailed comparison of data obtained from evolutionary and tumor studies supported this hypothesis since both germline and somatic mutations were found to occur preferentially at hypervariable sites of the D-loop. 24 The prevalence of transitions in tumor mtDNA would be compatible with oxidative DNA damage, [25][26][27][28] which is also discussed as a main source of mtDNA germline mutations. Enhanced oxidative damage in tumors could be caused by subtle alterations of the mitochondrial respiratory chain function.…”

Section: Discussionmentioning

confidence: 99%

High frequency of mitochondrial DNA mutations in glioblastoma multiforme identified by direct sequence comparison to blood samples

et al. 2001

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In an earlier study, we showed that heteroplasmy in the mitochondrial genome of gliomas sometimes occurs in a D-loop polycytosine tract. We extended this study by pairwise comparisons between glioma samples and adjacent brain tissue of 55 patients (50 glioblastomas, 1 astrocytoma WHO grade III, 4 astrocytomas WHO grade II). We used a combination of laser microdissection and PCR to detect and quantify variations in the polycytosine tract. New length variants undetectable in the adjacent brain tissue were observed in 5 glioblastomas (9%). In 2 of these cases, samples from a lower tumor stage (WHO grade II) could be analyzed and revealed the early occurrence of these mutations in both cases. Since the mitochondrial D-loop contains additional repeats and highly polymorphic non-coding sequences, we compared 17 glioblastomas with the corresponding blood samples of the same patients by direct sequencing of the complete D-loop. In 6 of these tumors (35%), instability was detected in 1 or 2 of 3 repeat regions; in 1 of these repeats, the instability was linked to a germline T-to-C transition. Furthermore, of 2 tumors (12%) 1 carried 1 and the other 9 additional transitions. In the latter patient, 6.7 kb of the protein coding mtDNA sequence were analyzed. Six silent transitions and 2 missense mutations (transitions) were found. All base substitutions appeared to be homoplasmic upon sequencing, and 89% occurred at known polymorphic sites in humans. Our data suggest that the same mechanisms that generate inherited mtDNA polymorphisms are strongly enhanced in gliomas and produce somatic mutations.

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Section: Discussionmentioning

confidence: 99%

High frequency of mitochondrial DNA mutations in glioblastoma multiforme identified by direct sequence comparison to blood samples

et al. 2001

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“…6 In spite of the intense work in this field, there is still complete lack of information regarding the time-scales at which cyclobutane dimers and (6-4) adducts are formed. Laser flash photolysis experiments, which provide such information, are difficult to perform for DNA components.…”

Section: Figurementioning

confidence: 99%

Time-Resolved Study of Thymine Dimer Formation

2005

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The formation of thymine dimers in the single-stranded oligonucleotide, (dT)20, is studied at room temperature by laser flash photolysis using 266 nm excitation. It is shown that the (6-4) adduct is formed within 4 ms via a reactive intermediate. The formation of cyclobutane dimers is faster than 200 ns. The overall quantum yield for the (6-4) formation is (3.7 ± 0.3) × 10-3, and that of the cyclobutane dimers is (2.8 ± 0.2) × 10-2. No triplet absorption is detected, showing that either the intersystem crossing yield decreases by 1 order of magnitude upon oligomerization (<1.4 × 10-3) or the triplet state reacts with unit efficiency in less than 200 ns to yield cyclobutane dimers.

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“…Several lines of evidence suggest that telomeres are especially susceptible to oxidative DNA damage [100,101], which may be the major source of DNA damage in mammalian organisms [102][103][104]. Finally, mutations that alter the expression or function of any of the telomere-associated proteins can also cause telomeres to malfunction.…”

Section: Mechanisms Of Telomere Disruptionmentioning

confidence: 99%

Cancer and aging: the importance of telomeres in genome maintenance

Rodier

Kim

Nijjar

et al. 2005

The International Journal of Biochemistry & Cell Biology

120

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Telomeres are the specialized DNA-protein structures that cap the ends of linear chromosomes, thereby protecting them from degradation and fusion by cellular DNA repair processes. In vertebrate cells, telomeres consist of several kilobase pairs of DNA having the sequence TTAGGG, a few hundred base pairs of single-stranded DNA at the 3' end of the telomeric DNA tract, and a host of proteins that organize the telomeric double and single stranded DNA into a protective structure.

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Oxidative damage to DNA: Formation, measurement, and biological significance

Cited by 267 publications

References 381 publications

High frequency of mitochondrial DNA mutations in glioblastoma multiforme identified by direct sequence comparison to blood samples

High frequency of mitochondrial DNA mutations in glioblastoma multiforme identified by direct sequence comparison to blood samples

Time-Resolved Study of Thymine Dimer Formation

Cancer and aging: the importance of telomeres in genome maintenance

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