Oxidative Decay of DNA

Abstract

The study of DNA oxidation has progressed from an exploratory phase, during which its basic biochemistry was established, into a field branching out into numerous areas. Early on, radiation biologists discovered that radiolysis of water generates oxygen free radicals, which are responsible for many of the consequences of irradiating living things. The characterization of radiation-induced oxidative DNA lesions, and the connection between radiation and cancer, caused a surge of interest in DNA oxidation per se and raised the possibility of DNA damage from biological oxidants. Nucleic acid biochemists, cancer biologists, and toxicologists then set out to ask key questions: "how much oxidative DNA damage is there, how does it get there, how and when is it removed, and what are the consequences?" A proliferation of techniques has resulted in the confirmation of the early hypotheses and also delivered some surprises. In this minireview, we have outlined some of the most interesting recent results. Extensive reviews on DNA oxidation published elsewhere have discussed the earlier work in detail (1-5). A companion minireview by Henle and Linn (6) covers in depth the biochemistry of DNA oxidation.

Clinical haematobiochemical parameters during experimental lead poisoning in goats: effects of methanol extract of Tiger nuts

“…The low values of packed cell volume, haemoglobin, total protein, and red blood cells obtained for the acute and chronic studies suggested that the administration of lead acetate causes anaemia. The result of this study agrees with the report of Beckman and Ames, (1997) who attributed the cause of anaemia due to lead toxicity to shortened erythrocyte lifespan and impairment of heme biosynthesis. Gani et al, (2017) also associated anaemia as a result of lead toxicosis to inhibition of activities of aminolevulinic acid dehydratase in haeme synthesis.…”

Clinical haematobiochemical parameters during experimental lead poisoning in goats: effects of methanol extract of Tiger nuts

“…The low values of packed cell volume, haemoglobin, total protein, and red blood cells obtained for the acute and chronic studies suggested that the administration of lead acetate causes anaemia. The result of this study agrees with the report of Beckman and Ames, (1997) who attributed the cause of anaemia due to lead toxicity to shortened erythrocyte lifespan and impairment of heme biosynthesis. Gani et al, (2017) also associated anaemia as a result of lead toxicosis to inhibition of activities of aminolevulinic acid dehydratase in haeme synthesis.…”

Involvement of Cytochrome B in Acute Rheumatic Fever and Rheumatic Heart Disease

“…In addition, there is not only a deficiency or absence of correction and repair systems in the mitochondrial genome, but also an apparent lack of recombination. Among mutations observed in patients, transversions (T) were less frequent than transitions (t) (60.32% versus 39.68%), and these were dominated at 63.16% by a mutation of C towards T. Our results agree with [22], that the general characteristics of mtDNA mutations are CT and AG transitions. However, frequency of transversions was greater in patients than in HC (11.38 against 0.34); in addition, although Ks was superior to Kns in patients, the latter was quite important (Ks = 0.009 +/-0.003, Kns = 0.006 +/-0.001) These results show that new mutations of MT-CYB (both transitions transversions) would have appeared in patients, demonstrating involvement of Cyt b nucleotide variations of in RHD.…”

Cytometric assessment of DNA damage by exogenous and endogenous oxidants reports aging‐related processes

“…Treatment with H 2 O 2 for even shorter (30 min) periods of time led to quite similar results (data not shown). The data are compatible with the known mechanism of induction of DNA damage by oxidants, which initially led to the formation of DNA SSLs, predominantly consisting of 8‐oxo‐dG, a fraction of which are converted into DSBs during DNA replication (1–8, 61). Since DSBs are the most potent inducers of ATM activation and H2AX phosphorylation (23–25) it is not surprising, therefore, that the S‐phase cells responded maximally to the short pulse of the oxidant (Fig.…”

Clinical haematobiochemical parameters during experimental lead poisoning in goats: effects of methanol extract of Tiger nuts

“…The low values of packed cell volume, haemoglobin, total protein, and red blood cells obtained for the acute and chronic studies suggested that the administration of lead acetate causes anaemia. The result of this study agrees with the report of Beckman and Ames, (1997) who attributed the cause of anaemia due to lead toxicity to shortened erythrocyte lifespan and impairment of heme biosynthesis. Gani et al, (2017) also associated anaemia as a result of lead toxicosis to inhibition of activities of aminolevulinic acid dehydratase in haeme synthesis.…”

Involvement of Cytochrome B in Acute Rheumatic Fever and Rheumatic Heart Disease

“…In addition, there is not only a deficiency or absence of correction and repair systems in the mitochondrial genome, but also an apparent lack of recombination. Among mutations observed in patients, transversions (T) were less frequent than transitions (t) (60.32% versus 39.68%), and these were dominated at 63.16% by a mutation of C towards T. Our results agree with [22], that the general characteristics of mtDNA mutations are CT and AG transitions. However, frequency of transversions was greater in patients than in HC (11.38 against 0.34); in addition, although Ks was superior to Kns in patients, the latter was quite important (Ks = 0.009 +/-0.003, Kns = 0.006 +/-0.001) These results show that new mutations of MT-CYB (both transitions transversions) would have appeared in patients, demonstrating involvement of Cyt b nucleotide variations of in RHD.…”

Cytometric assessment of DNA damage by exogenous and endogenous oxidants reports aging‐related processes

“…Treatment with H 2 O 2 for even shorter (30 min) periods of time led to quite similar results (data not shown). The data are compatible with the known mechanism of induction of DNA damage by oxidants, which initially led to the formation of DNA SSLs, predominantly consisting of 8‐oxo‐dG, a fraction of which are converted into DSBs during DNA replication (1–8, 61). Since DSBs are the most potent inducers of ATM activation and H2AX phosphorylation (23–25) it is not surprising, therefore, that the S‐phase cells responded maximally to the short pulse of the oxidant (Fig.…”

Clinical haematobiochemical parameters during experimental lead poisoning in goats: effects of methanol extract of Tiger nuts

“…The low values of packed cell volume, haemoglobin, total protein, and red blood cells obtained for the acute and chronic studies suggested that the administration of lead acetate causes anaemia. The result of this study agrees with the report of Beckman and Ames, (1997) who attributed the cause of anaemia due to lead toxicity to shortened erythrocyte lifespan and impairment of heme biosynthesis. Gani et al, (2017) also associated anaemia as a result of lead toxicosis to inhibition of activities of aminolevulinic acid dehydratase in haeme synthesis.…”

Involvement of Cytochrome B in Acute Rheumatic Fever and Rheumatic Heart Disease

“…In addition, there is not only a deficiency or absence of correction and repair systems in the mitochondrial genome, but also an apparent lack of recombination. Among mutations observed in patients, transversions (T) were less frequent than transitions (t) (60.32% versus 39.68%), and these were dominated at 63.16% by a mutation of C towards T. Our results agree with [22], that the general characteristics of mtDNA mutations are CT and AG transitions. However, frequency of transversions was greater in patients than in HC (11.38 against 0.34); in addition, although Ks was superior to Kns in patients, the latter was quite important (Ks = 0.009 +/-0.003, Kns = 0.006 +/-0.001) These results show that new mutations of MT-CYB (both transitions transversions) would have appeared in patients, demonstrating involvement of Cyt b nucleotide variations of in RHD.…”

Cytometric assessment of DNA damage by exogenous and endogenous oxidants reports aging‐related processes

“…Treatment with H 2 O 2 for even shorter (30 min) periods of time led to quite similar results (data not shown). The data are compatible with the known mechanism of induction of DNA damage by oxidants, which initially led to the formation of DNA SSLs, predominantly consisting of 8‐oxo‐dG, a fraction of which are converted into DSBs during DNA replication (1–8, 61). Since DSBs are the most potent inducers of ATM activation and H2AX phosphorylation (23–25) it is not surprising, therefore, that the S‐phase cells responded maximally to the short pulse of the oxidant (Fig.…”