Mechanism for manganese enhancement of dopamine-induced oxidative DNA damage and neuronal cell death

Oikawa, Shinji; Hirosawa, Iwao; Tada‐Oikawa, Saeko; Furukawa, Ayako; Nishiura, Kaoru; Kawanishi, Shosuke

doi:10.1016/j.freeradbiomed.2006.05.018

Cited by 54 publications

(46 citation statements)

References 49 publications

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“…The enhancing effect of SOD on the DNA damage induced by Cu(II) and H 2 O 2 has been reported. 21 16) We showed for the first time that Mn(II) enhanced the oxidative DNA damage induced by Cu(II) more effectively than that induced by Fe(III)-NTA in the presence of dopamine. Cu(II) is closely located to DNA, and its reduced form Cu(I) tightly binds to DNA and introduces a conformational change.…”

Section: Discussionmentioning

confidence: 87%

“…24) The bound Cu(I) anchors the H 2 O 2 that attacks DNA by forming a DNA-Cu(I)-OOH complex. 16) In contrast, Fe(III)-NTA provides hydroxyl radicals far from DNA. Therefore, the accelerated supply of H 2 O 2 by Mn(II) may have enhanced the DNA damage in the Cu(II)-dopamine system compared to that in the Fe(III)-NTA.…”

Section: Discussionmentioning

confidence: 99%

“…Dopamine-induced oxidative DNA damage or cytotoxicity in the presence of Cu(II) is enhanced by Mn(II). 16,17) However, in those studies, the di- (8-oxodG), xanthine oxidase, and 2 -deoxyguanosine (dG) were purchased from Sigma (St. Louis, MO, U.S.A.). Sulfanilic acid and hydroxyl ammonium were obtained from Kanto Chemical Co. (Tokyo, Japan).…”

Section: Introductionmentioning

confidence: 99%

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Combined Effects of Manganese, Iron, Copper, and Dopamine on Oxidative DNA Damage

Ando

Ueda

Okamoto

et al. 2011

JOURNAL OF HEALTH SCIENCE

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Combined Effects of Manganese, Iron, Copper, and Dopamine on Oxidative DNA Damage

Ando

Ueda

Okamoto

et al. 2011

JOURNAL OF HEALTH SCIENCE

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“…may also be involved with dopaminergic toxicity. Oikawa et al (2006) found that PC12 cells exposed independently to either 0.2 mM Mn 2? or DA did not change significantly; however, when cells were co-exposed to Mn and DA, cell death was induced by a mechanism involving DNA damage.…”

Section: Manganese Mitochondria and Oxidative Damagementioning

confidence: 96%

Manganese accumulation in the CNS and associated pathologies

2011

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Manganese (Mn) is an essential metal for life. It is a key constituent of clue enzymes in the central nervous system, contributing to antioxidant defenses, energetic metabolism, ammonia detoxification, among other important functions. Until now, Mn transport mechanisms are partially understood; however, it is known that it shares some mechanisms of transport with iron. CNS is susceptible to Mn toxicity because it possesses mechanisms that allow Mn entry and favor its accumulation. Cases of occupational Mn exposure have been extensively reported in the literature; however, there are other ways of exposure, such as long-term parental nutrition and liver failure. Manganism and hepatic encephalopathy are the most common pathologies associated with the effects of Mn exposure. Both pathologies are associated with motor and psychiatric disturbances, related in turn to mechanisms of damage such as oxidative stress and neurotransmitters alterations, the dopaminergic system being one of the most affected. Although manganism and Parkinson's disease share some characteristics, they differ in many aspects that are discussed here. The mechanisms for Mn transport and its participation in manganism and hepatic encephalopathy are also considered in this review. It is necessary to find an effective therapeutic strategy to decrease Mn levels in exposed individuals and to treat Mn long term effects. In the case of patients with chronic liver failure it would be worthwhile to test a low-Mn diet in order to ameliorate symptoms of hepatic encephalopathy possibly related to Mn accumulation.

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“…1,2) Oikawa et al showed a possible link between copper-mediated oxidative DNA damage and dopaminergic neuronal cell death. 3) Several groups including us proposed mechanisms for the oxidative DNA damage induced by copper and catechol compounds. 4,5) However, the detailed mechanisms remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Involvement of DNA Conformational Change Induced by Rearrangement of Copper-coordination Geometry in Oxidative DNA Damages Caused by Copper and Dopamine

Ando

Ueda

Makino

et al. 2009

JOURNAL OF HEALTH SCIENCE

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Oxidative DNA damages involve reductionoxidation reactions between certain metals and compounds, and result in genetic abnormalities leading to diseases including cancer and neurodegenerative disorders. Here, we report that DNA damages mediated by combination of a neurotransmitter dopamine and copper accompany a unique DNA conformational change. Copper(II) [Cu(II)] was shown as bound to consecutive guanines (G-G) of DNA, by demonstrating the G-G selective inhibition of restriction enzymes. When dopamine was added to calf thymus DNA in the presence of Cu(II), DNA guanines were oxidized. UV and 1 H NMR analyses suggested that dopamine was oxidized to the quinone form in the presence of Cu(II). The circular dichroism experiments showed DNA spectral changes under the conditions of oxidative DNA damage, indicating a conformational change of the DNA strand by dopamine and copper. The DNA conformational change was suppressed by adding a Cu(I)-specific chelator bathocuproine. Therefore, the conformational change can be explained by a rearrangement of the copper-coordination geometry in DNA through Cu(II) reduction to Cu(I). Thus, changes in DNA conformation could be involved in metal-mediated genotoxicity as well as oxidative damage but via different mechanism.

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Mechanism for manganese enhancement of dopamine-induced oxidative DNA damage and neuronal cell death

Cited by 54 publications

References 49 publications

Combined Effects of Manganese, Iron, Copper, and Dopamine on Oxidative DNA Damage

Combined Effects of Manganese, Iron, Copper, and Dopamine on Oxidative DNA Damage

Manganese accumulation in the CNS and associated pathologies

Involvement of DNA Conformational Change Induced by Rearrangement of Copper-coordination Geometry in Oxidative DNA Damages Caused by Copper and Dopamine

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