Spontaneous and 2-nitropropane induced levels of 8-hydroxy-2'-deoxyguanosine in liver DNA of rats fed iron-deficient or manganese- and copper-deficient diets

Adachi, Shuichi; Takemoto, Kazuo; Hirosue, Toshiko; Hosogai, Yuutaro

doi:10.1093/carcin/14.2.265

Cited by 14 publications

(9 citation statements)

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“…Iron deficiency can induce nuclear DNA base damage (33). Whereas every-third-day-supplemented rats had levels of mtDNA damage that were not significantly higher than ironnormal rats on the second and third day after treatment, daily high-iron-supplemented rats had damage that was significantly different from iron-normal rats.…”

Section: Figmentioning

confidence: 85%

Iron deficiency and iron excess damage mitochondria and mitochondrial DNA in rats

Walter

Knutson

Paler-Martı́nez

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

301

182

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Approximately two billion people, mainly women and children, are iron deficient. Two studies examined the effects of iron deficiency and supplementation on rats. In study 1, mitochondrial functional parameters and mitochondrial DNA (mtDNA) damage were assayed in iron-deficient (<5 g͞day) and iron-normal (800 g͞day) rats and in both groups after daily high-iron supplementation (8,000 g͞day) for 34 days. This dose is equivalent to the daily dose commonly given to iron-deficient humans. Iron-deficient rats had lower liver mitochondrial respiratory control ratios and increased levels of oxidants in polymorphonuclear-leukocytes, as assayed by dichlorofluorescein (P < 0.05). Rhodamine 123 fluorescence of polymorphonuclear-leukocytes also increased (P < 0.05). Lowered respiratory control ratios were found in daily high-iron-supplemented rats regardless of the previous iron status (P < 0.05). mtDNA damage was observed in both iron-deficient rats and rats receiving daily high-iron supplementation, compared with ironnormal rats (P < 0.05). Study 2 compared iron-deficient rats given high doses of iron (8,000 g) either daily or every third day and found that rats given iron supplements every third day had less mtDNA damage on the second and third day after the last dose compared to daily high iron doses. Both inadequate and excessive iron (10 ؋ nutritional need) cause significant mitochondrial malfunction. Although excess iron has been known to cause oxidative damage, the observation of oxidant-induced damage to mitochondria from iron deficiency has been unrecognized previously. Untreated iron deficiency, as well as excessive-iron supplementation, are deleterious and emphasize the importance of maintaining optimal iron intake.

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Section: Figmentioning

confidence: 85%

Iron deficiency and iron excess damage mitochondria and mitochondrial DNA in rats

Walter

Knutson

Paler-Martı́nez

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

301

182

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“…Administration of chemical carcinogens [1,2] or irradiation of Á-or X-rays [3] induces accumulation of 8-oxodG residues in the tissues of experimental animals. Furthermore, the accumulation of 8-oxodG in cultured cells [4], aged rats [5] and humans [6,7] has been reported.…”

Section: Introductionmentioning

confidence: 99%

Accumulation of 8-Oxo-2’-Deoxyguanosine (as a Biomarker of Oxidative DNA Damage) in the Tissues of Aged Hamsters and Change in Antioxidant Enzyme Activities after Single Administration of N-Nitrosobis(2-Oxopropyl) Amine

et al. 2004

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Background: It has been reported that DNA oxidative damage accumulates with age. Two reasons for this phenomenon are the decline in the antioxidant system and the decline in the repair system. It is not clear which of these is the main reason. Objective: To study whether the decline in antioxidant enzyme activities causes the accumulation of DNA oxidative damage, an experimental study was performed with hamsters. Methods: Seventy-four female Syrian golden hamsters were divided into 2 groups: a young group (28 hamsters), and an aged group (46 hamsters). The hamsters in the aged group were kept in our laboratory until they were 18 months old. The levels of 8-oxo-2′-deoxyguanosine (8-oxodG) and the activities of antioxidant enzymes, i.e. catalase, superoxide dismutase (SOD), and glutathione peroxidase (GPx), were measured in both groups. Furthermore, the same parameters were measured in the pancreas and liver following administration of N-nitrosobis(2-oxopropyl)amine (BOP), an inducer of oxidative stress in the hamster pancreas. Results: In the mid brain, cerebellum, lung, heart, spleen and kidney, the 8-oxodG contents in aged hamsters were significantly higher than those in young hamsters. GPx activity decreased with age in the lung, liver and kidney, whereas SOD activity increased in the lung and liver but decreased in the kidney of aged animals. Catalase activity increased in the cerebrum, heart, pancreas and kidney but decreased in the lung and spleen of aged hamsters. When the pancreatic levels of 8-oxodG and antioxidant enzymes were measured after BOP administration, there was no clear-cut relation between the changes in those levels. Conclusions: From these results the increase in 8-oxodG contents in aged hamsters does not seem to be related to the antioxidant system but rather to a possible decline in the repair system against oxidative damage.

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“…The level of SCEs in lymphocytes from IDA patients was significantly lower (∼20% less) than that observed in the control group (3.788 ± 0.11 vs. 4.720 ± 0.18, respectively, P < 0.001). This decrease in SCEs in IDA patients was not expected because previous studies have shown that IDA is associated with a high level of oxidants and reduced total antioxidant capacity [17][18][19]27].…”

Section: Resultsmentioning

confidence: 75%

“…In addition, DNA damage is significantly correlated with the severity of oxidative stress and anemia [17]. High levels of 8-hydroxy-2 -deoxyguanosine and mitochondrial DNA double strand breaks were reported in rats with IDA [18,19]. This damage was proposed to be induced by the high oxidant levels associated with IDA.…”

Section: Discussionmentioning

confidence: 99%

“…Aslan et al [17] reported an increase in DNA damage in lymphocytes from IDA patients using an alkaline comet assay. In animal studies, rats with IDA showed increased oxidative damage to both nuclear and mitochondrial DNA; the increased oxidative damage was attributed to the high levels of oxidants found in cells and the reduced activities of oxidative enzymes, cytochromes and iron-sulfur proteins [18,19]. Therefore, in the current study, genotoxicity in the lymphocytes of IDA patients was examined using sister chromatid exchanges (SCEs) and chromosomal aberrations (CAs) assays.…”

Section: Introductionmentioning

confidence: 95%

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Genotoxicity assessment in iron deficiency anemia patients using sister chromatid exchanges and chromosomal aberrations assays

Khabour

Soudah

Aaysh

2013

Mutation Research/Genetic Toxicology and Environmental Mutagene

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Spontaneous and 2-nitropropane induced levels of 8-hydroxy-2'-deoxyguanosine in liver DNA of rats fed iron-deficient or manganese- and copper-deficient diets

Cited by 14 publications

References 0 publications

Iron deficiency and iron excess damage mitochondria and mitochondrial DNA in rats

Iron deficiency and iron excess damage mitochondria and mitochondrial DNA in rats

Accumulation of 8-Oxo-2’-Deoxyguanosine (as a Biomarker of Oxidative DNA Damage) in the Tissues of Aged Hamsters and Change in Antioxidant Enzyme Activities after Single Administration of N-Nitrosobis(2-Oxopropyl) Amine

Genotoxicity assessment in iron deficiency anemia patients using sister chromatid exchanges and chromosomal aberrations assays

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