Oxidative DNA damage (8-hydroxydeoxyguanosine) and body iron status: a study on 2507 healthy people

Nakano, Masaru; Kawanishi, Yasuo; Kamohara, Seika; Uchida, Yoshiko; Shiota, M; Inatomi, Yuka; Komori, Toyonori; Miyazawa, Katsumi; Gondo, Kazumi; Yamasawa, I.

doi:10.1016/s0891-5849(03)00432-5

Cited by 89 publications

(70 citation statements)

References 30 publications

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“…Furthermore, this increased excretion was reversable by phlebotomy, giving further support for body iron as the major determinant [22]. The only other study relating body iron with oxidative DNA damage in healthy subjects was conducted in 2507 men and women in Tokyo, Japan [10]. In that study, Nakano and coworkers observed almost no change by age in urinary 8-OHdG excretion in males, but did observe an age-dependent increase in the excretion rate in women, most marked at the time of menopause.…”

Section: Discussionmentioning

confidence: 88%

“…They also observed a statistically significant direct correlation between serum ferritin concentration and urinary 8-OHdG excretion rate [10].…”

Section: Introductionmentioning

confidence: 84%

“…Recently, Nakano and coworkers studied urinary 8-OHdG excretion in 2507 healthy Japanese and showed an age-dependent gender difference so that pre-menopausal females had lower and post-menopausal females higher 8-OHdG excretion rate as compared with males of the same age [10]. They also observed a statistically significant direct correlation between serum ferritin concentration and urinary 8-OHdG excretion rate [10].…”

Section: Introductionmentioning

confidence: 98%

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Body iron is a contributor to oxidative damage of DNA

Tuomainen

Loft

Nyyssönen

et al. 2007

Free Radical Research

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The transition metal iron is catalytically highly active in vitro, and not surprisingly, body iron has been suggested to promote oxidative stress in vivo. In the current analysis we studied the association of serum ferritin concentration and serum soluble transferrin receptor concentration with daily urinary 8-hydroxydeoxyguanosine excretion, a marker of oxidative stress, in 48 mildly dyslipidemic men in East Finland. In multivariate linear regression analyses allowing for age, smoking, body mass index and physical exercise, serum ferritin concentration predicted the excretion rate at B ¼ 0.17 (95% CI 0.08-0.26, P ¼ 0.001), and serum soluble transferrin receptor to ferritin concentration ratio (TfR/ferritin) predicted the excretion rate at B ¼ 20.13 (95% CI 2 0.21 to 20.05, P ¼ 0.002). Our data suggest that body iron contributes to excess oxidative stress already at noniron overload concentrations in these subjects.

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Section: Discussionmentioning

confidence: 88%

“…They also observed a statistically significant direct correlation between serum ferritin concentration and urinary 8-OHdG excretion rate [10].…”

Section: Introductionmentioning

confidence: 84%

Section: Introductionmentioning

confidence: 98%

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Body iron is a contributor to oxidative damage of DNA

Tuomainen

Loft

Nyyssönen

et al. 2007

Free Radical Research

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“…Increased iron could lead to oxidative stress and sensitize the skin to UV exposure. Urinary levels of 8-oxo-2'-deoxyguanosine, a marker of oxidative DNA adducts, has been shown to increase with serum ferritin levels in men and women (26). Because iron is a growth nutrient, increased iron could also increase proliferation of osteoblast progenitors without differentiation to mature osteoblasts and thus, slow bone formation.…”

Section: Iron and Menopause 2941mentioning

confidence: 99%

Iron and Menopause: Does Increased Iron Affect the Health of Postmenopausal Women?

Jian

Pelle

Huang

2009

Antioxidants & Redox Signaling

136

125

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Estrogen deficiency has been regarded as the main causative factor in menopausal symptoms and diseases. Here, we show that although estrogen decreases by 90%, a concurrent but inverse change occurs in iron levels during menopausal transition. For example, levels of serum ferritin are increased by two-to threefold from before menopause to after menopause. This observation has led us to hypothesize that, in addition to estrogen deficiency, increased iron as a result of menopause could be a risk factor affecting the health of postmenopausal women. Further studies on iron and menopause are clinically relevant and may provide novel therapeutic treatments.

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“…1,[3][4][5] More subtle differences of higher iron burden in populations have also been linked with liver and cardiovascular disease, diabetes, cancer, increased oxidative DNA damage, and neurodegenerative disorders. [6][7][8][9][10][11] In addition, the iron status of a host may be a major factor in infections, 12 and iron deficiencies associated with anemias are of wide concern. 13 The absorption of iron and its subsequent use and turnover are highly regulated and likely to be influenced by individual variation.…”

mentioning

confidence: 99%

Multiple polymorphic loci determine basal hepatic and splenic iron status in mice

Grant¹,

Robinson²,

Edwards³

et al. 2006

Hepatology

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Polymorphisms of genes linked to iron metabolism may account for individual variability in hemochromatosis and iron status connected with liver and cardiovascular diseases, cancers, toxicity, and infection. Mouse strains exhibit marked differences in levels of non-heme iron, with C57BL/6J and SWR showing low and high levels, respectively. The genetic basis for this variability was examined using quantitative trait loci (QTL) analysis together with expression profiling and chromosomal positions of known iron-related genes. Non-heme iron levels in liver and spleen of C57BL/6J ؋ SWR F 2 mice were poorly correlated, indicating independent regulation. Highly significant (P < .01) polymorphic loci were found on chromosomes 2 and 16 for liver and on chromosomes 8 and 9 for spleen. With sex as a covariate, additional significant or suggestive (P < 0.1) QTL were detected on chromosomes 7, 8, 11, and 19 for liver and on chromosome 2 for spleen. A gene array showed no clear association between most loci and differential iron-related gene expression. The gene for transferrin and a transferrin-like gene map close to the QTL on chromosome 9. Transferrin saturation was significantly lower in C57BL/6J mice than in SWR mice, but there was no significant difference in the serum level of transferrin, hepatic expression, or functional change in cDNA sequence. ␤2-Microglobulin, which, unlike other loci, was associated with C57BL/6J alleles, is a candidate for the chromosome 2 QTL for higher iron. In conclusion, the findings show the location of polymorphic genes that determine basal iron status in wild-type mice. Human equivalents may be pertinent in predisposition to hepatic and other disorders. (HEPATOLOGY 2006;44:174-185.)

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Oxidative DNA damage (8-hydroxydeoxyguanosine) and body iron status: a study on 2507 healthy people

Cited by 89 publications

References 30 publications

Body iron is a contributor to oxidative damage of DNA

Body iron is a contributor to oxidative damage of DNA

Iron and Menopause: Does Increased Iron Affect the Health of Postmenopausal Women?

Multiple polymorphic loci determine basal hepatic and splenic iron status in mice

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