• Bulletin of the Korean Chemical Society
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• v.26 no.8
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• pp.1255-1259
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• 2005

Lewy bodies (LBs) are neuronal inclusions that are closely related to Parkinson's disease (PD). The filamentous component of LB from patients with PD contains biochemically altered $\alpha$-synuclein. We have investigated the effect of the oxidized products of catecholamines on the modification of $\alpha$-synuclein. When $\alpha$-synuclein was incubated with the oxidized 3,4-dihydroxyphenylalanine (L-DOPA) or dopamine, the protein was induced to be aggregated. The oxidized catecholamine-mediated $\alpha$-synuclein aggregation was enhanced by copper ion. Radical scavengers, azide and N-acetyl cysteine significantly prevented the oxidized catecholamine-mediated $\alpha$-synuclein aggregation. The results suggest that free radical may play a role in $\alpha$-synuclein aggregation. Exposure of $\alpha$-synuclein to the oxidized products of catecholamines led to the formation of dityrosine. Antioxidant dipeptides carnosine, homocarnosine and anserine significantly protected $\alpha$-synuclein from the aggregation induced by the oxidized products of catecholamines.

• BMB Reports
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• v.43 no.3
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• pp.219-224
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• 2010

Lipid peroxidation is known to be an important factor in the pathologies of many diseases associated with oxidative stress. We assessed the lipid peroxidation induced by the reaction of ferritin with $H_2O_2$. When linoleic acid micelles or phosphatidyl choline liposomes were incubated with ferritin and $H_2O_2$, lipid peroxidation increased in the presence of ferritin and $H_2O_2$ in a concentration-dependent manner. The hydroxyl radical scavengers, azide and thiourea, prevented lipid peroxidation induced by the ferritin/$H_2O_2$ system. The iron specific chelator desferoxamine also prevented ferritin/$H_2O_2$ systemmediated lipid peroxidation. These results demonstrate the possible role of iron in ferritin/$H_2O_2$ system-mediated lipid peroxidation. Carnosine is involved in many cellular defense processes, including free radical detoxification. In this study, carnosine, homocarnosine, and anserine were shown to significantly prevent ferritin/$H_2O_2$ system-mediated lipid peroxidation and also inhibited the free radical-generation activity of ferritin. These results indicated that carnosine and related compounds may prevent ferritin/$H_2O_2$ system-mediated lipid peroxidation via free radical scavenging.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.3
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• pp.251-261
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• 1999

The effects of carnosine and related compounds (CRCs) including anserine, homocarnosine, histidine, and ${\beta}-alanine$ on monosaccharide autoxidation and $H_2O_2$ formation were investigated. The incubation of CRCs with D-glucose, D-glucosamine, and D, L-glyceraldehyde at $37^{\circ}C$ increased the absorption maxima at 285 nm, 273 nm, and $290{\sim}330$ nm, respectively. D, L-glyceraldehyde was the most reactive sugar with CRCs. The presence of copper strongly stimulated the reaction of carnosine and anserine with D-glucose or D-glucosamine. Carnosine and anserine stimulated $H_2O_2$ formation from D-glucose autoxidation in a dose-dependent manner in the presence of 10 ${\mu}M$ Cu (II). The presence of human serum albumin (HSA) decreased their effect on $H_2O_2$ formation. Carnosine and anserine has a biphasic effect on ${\alpha}-ketoaldehyde$ formation from glucose autoxidation. CRCs inhibited glycation of HSA as determined by hydroxymethyl furfural, lysine residue with free ${\varepsilon}-amino$ group, and fructosamine assay. These results suggest that CRCs may be protective against diabetic complications by reacting with sugars and protecting glycation of protein.