Protective effects of carnosine and homocarnosine on ferritin and hydrogen peroxide-mediated DNA damage

Kang, Jung-Hoon

doi:10.3858/bmbrep.2010.43.10.683

Cited by 6 publications

(12 citation statements)

References 29 publications

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“…The main characteristic of antioxidants is the ability to trap free radicals. 27 In our study, administration of carnosine at a dose of 100 mg kg -1 before injection to CP reduced the frequency of MnPCE almost 3.76-fold. 1,5 It appears that the primary defence mechanism of chemoprotective agent is directly and/or indirectly interaction with these ROS.…”

Section: Discussionsupporting

confidence: 52%

“…26 Kang et al showed that carnosine effectively inhibited ferritin/H 2 O 2 -mediated hydroxyl radical generation and decreased the mutagenicity of DNA. 27 In our study, administration of carnosine at a dose of 100 mg kg -1 before injection to CP reduced the frequency of MnPCE almost 3.76-fold. Carnosine has protective efficacy more than other natural products that we have tested in our laboratory.…”

Section: Discussionsupporting

confidence: 52%

“…1,5 It appears that the primary defence mechanism of chemoprotective agent is directly and/or indirectly interaction with these ROS. 27 The antioxidant activity of this molecule may involve reduction of oxidative potential or stabilization of the imidazole radical, probably due to the peptide bond. 19 The secondary protection of carnosine is involved in increasing cellular antioxidant enzymes such as glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) activities.…”

Section: Discussionmentioning

confidence: 99%

“…DPPH is a large molecule compare with free hydroxyl radical that previously was reported to inhibit this small free radical (OH) by carnosine. 27 The antioxidant activity of this molecule may involve reduction of oxidative potential or stabilization of the imidazole radical, probably due to the peptide bond. 19 Chelation of transition metals such as iron or copper may be important for antioxidant activity of carnosine.…”

Section: Discussionmentioning

confidence: 99%

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Chemoprotective effects of carnosine against genotoxicity induced by cyclophosphamide in mice bone marrow cells

Naghshvar

Abianeh

Ahmadashrafi

et al. 2012

Cell Biochemistry & Function

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The protective effects of carnosine as a natural dipeptide were investigated in mouse bone marrow cells against genotoxicity induced by cyclophosphamide. Mice were injected with solutions of carnosine at three different doses (10, 50 and 100 mg kg(-1) bw) for five consecutive days. On the fifth day of treatment, mice were injected cyclophosphamide and killed after 24 h. The frequency of micronuclei in polychromatic erythrocytes and the ratio of polychromatic erythrocyte/polychromatic erythrocyte + normochromatic erythrocyte [PCE/(PCE + NCE)] were evaluated by May-Grunwald/Giemsa staining. Histopathology of bone marrow was examined in mice treated with cyclophosphamide and carnosine. Carnosine significantly reduced micronucleated polychromatic erythrocytes (MnPCEs) induced by cyclophosphamide at all three doses. Carnosine at dose of 100 mg kg(-1) bw reduced MnPCEs 3.76-fold and completely normalized the PCE/(PCE + NCE) ratio. Administration of carnosine inhibited bone marrow toxicity induced by cyclophosphamide. It appeared that carnosine with protective activity reduced the oxidative stress and genotoxicity induced by cyclophosphamide in bone marrow cells of mice.

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Section: Discussionsupporting

confidence: 52%

Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Chemoprotective effects of carnosine against genotoxicity induced by cyclophosphamide in mice bone marrow cells

Naghshvar

Abianeh

Ahmadashrafi

et al. 2012

Cell Biochemistry & Function

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“…Since iron was the best transition metal to promote Fenton's reaction in vitro and apparently in vivo , we tested the possibility that CN stimulation of Fenton's reaction in vivo was specific to our readout, which was (chromosomal) DNA. Plasmid relaxation is a convenient and sensitive DNA‐based readout for Fenton's reaction in vitro (Park and Imlay, ; Surguladze et al ., ; Kang, ). Remarkably, in contrast to CN inhibition of the classic in vitro Fenton's reaction (Fig.…”

Section: Resultsmentioning

confidence: 98%

Cyanide enhances hydrogen peroxide toxicity by recruiting endogenous iron to trigger catastrophic chromosomal fragmentation

Mahaseth

Kuzminov

2015

Molecular Microbiology

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Hydrogen peroxide (HP) or cyanide (CN) are bacteriostatic at low-millimolar concentrations for growing Escherichia coli, whereas CN+HP mixture is strongly bactericidal. We show that this synergistic toxicity is associated with catastrophic chromosomal fragmentation. Since CN-alone does not kill at any concentration, while HP-alone kills at 20 mM, CN must potentiate HP poisoning. The CN+HP killing is blocked by iron chelators, suggesting Fenton’s reaction. Indeed, we show that CN enhances plasmid DNA relaxation due to Fenton’s reaction in vitro. However, mutants with elevated iron or HP pools are not acutely sensitive to HP-alone treatment, suggesting that, in addition, in vivo CN recruits iron from intracellular depots. We found that part of the CN-recruited iron pool is managed by ferritin and Dps: ferritin releases iron on cue from CN, while Dps sequesters it, quelling Fenton’s reaction. We propose that disrupting intracellular iron trafficking is a common strategy employed by the immune system to kill microbes.

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Prophylactic administration of carnosine and melatonin abates the incidence of renal toxicity induced by an over dose of titanium dioxide nanoparticles

Fadda

Mohamed

Ali

et al. 2018

J Biochem & Molecular Tox

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The alleviative effects of two antioxidants, carnosine (Car) and melatonin (Mel), against titanium dioxide nanoparticles (TiO -NPs) toxicity-induced oxidative and inflammatory renal damage were examined in rats. Administration of these antioxidants along with TiO -NPs effectively reduced serum urea, uric acid, creatinine, glucose, tumor necrosis factor-α, interleukin-6, C-reactive protein, immunoglobulin G, vascular endothelial growth factor, and nitric oxide, as well as a significant amelioration of the decrease in glutathione levels in renal tissue was observed, compared to those in rats treated with TiO -NPs alone. The renoprotective properties of the antioxidants were confirmed by reduced intensity of renal damage as demonstrated by histological findings. In conclusion, Car and Mel play protective roles against TiO -NPs-induced renal inflammation and oxidative injury, likely due to their antioxidant and anti-inflammatory properties.

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Protective effects of carnosine and homocarnosine on ferritin and hydrogen peroxide-mediated DNA damage

Cited by 6 publications

References 29 publications

Chemoprotective effects of carnosine against genotoxicity induced by cyclophosphamide in mice bone marrow cells

Chemoprotective effects of carnosine against genotoxicity induced by cyclophosphamide in mice bone marrow cells

Cyanide enhances hydrogen peroxide toxicity by recruiting endogenous iron to trigger catastrophic chromosomal fragmentation

Prophylactic administration of carnosine and melatonin abates the incidence of renal toxicity induced by an over dose of titanium dioxide nanoparticles

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