Differences in the antioxidant mechanism of carnosine in the presence of copper and iron

Decker, Eric A.; Crum, Andrea D.; Calvert, John T.

doi:10.1021/jf00017a009

Cited by 137 publications

(69 citation statements)

References 15 publications

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“…Our results also suggest that the modification at proline residues is the primary cause for the abnormal filament assembly of NF-L. Previous in vitro and in vivo studies have shown that carnosine possesses antioxidant properties, cytosolic buffering functions, metal chelating capabilities and may function as a wound healing agent (34)(35)(36)(37). In this study, we found that carnosine and anserine significantly inhibited NF-L aggregation induced by salsolinol (Fig.…”

Section: Resultssupporting

confidence: 75%

Salsolinol, a tetrahydroisoquinoline-derived neurotoxin, induces oxidative modification of neurofilament-L: protection by histidyl dipeptides

Kang¹

2012

BMB Reports

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Salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline) is a compound derived from dopamine metabolism and is capable of causing dopaminergic neurodegeneration. Oxidative modification of neurofilament proteins has been implicated in the pathogenesis of neurodegenerative disorders. In this study, oxidative modification of neurofilament-L (NF-L) by salsolinol and the inhibitory effects of histidyl dipeptides on NF-L modification were investigated. When NF-L was incubated with 0.5 mM salsolinol, the aggregation of protein was increased in a time-dependent manner. We also found that the generation of hydroxyl radicals (•OH) was linear with respect to the concentrations of salsolinol as a function of incubation time. NF-L exposure to salsolinol produced losses of glutamate, lysine and proline residues. These results suggest that the aggregation of NF-L by salsolinol may be due to oxidative damage resulting from free radicals. Carnosine, histidyl dipeptide, is involved in many cellular defense processes, including free radical detoxification.

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Section: Resultssupporting

confidence: 75%

Salsolinol, a tetrahydroisoquinoline-derived neurotoxin, induces oxidative modification of neurofilament-L: protection by histidyl dipeptides

Kang¹

2012

BMB Reports

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“…Many functions have previously been proposed for carnosine, including as an antioxidant and free radical scavenger, physiological buffer, neurotransmitter, radioprotectant, metal chelator and wound healing agent (21)(22)(23)(24). In the present study, it was found that carnosine and homocarnosine significantly inhibited DNA strand breakage induced by the ferritin/H2O2 system (Fig.…”

Section: Resultssupporting

confidence: 62%

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

Kang

2010

BMB Reports

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“…Carnosine and related compounds are reported to be the active free radical scavenger. 20,21 Effect of carnosine, homocarnosine and anserine on MG/lysine/Fe 3+ -mediated DNA cleavage was investigated. These compounds showed a concentration-dependent inhibition of DNA cleavage induced by MG/lysine/Fe 3+ (Fig.…”

Section: Resultsmentioning

confidence: 99%

Protective Effects of Carnosine and Relative Compounds on DNA Cleavage by Advanced Glycation End Products

Kang¹

2005

Bulletin of the Korean Chemical Society

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Differences in the antioxidant mechanism of carnosine in the presence of copper and iron

Cited by 137 publications

References 15 publications

Salsolinol, a tetrahydroisoquinoline-derived neurotoxin, induces oxidative modification of neurofilament-L: protection by histidyl dipeptides

Salsolinol, a tetrahydroisoquinoline-derived neurotoxin, induces oxidative modification of neurofilament-L: protection by histidyl dipeptides

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

Protective Effects of Carnosine and Relative Compounds on DNA Cleavage by Advanced Glycation End Products

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