Molecular & Cellular Toxicology

  • 제5권2호
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  • Pages.108-112
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  • 2009
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  • 1738-642X(pISSN)
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  • 2092-8467(eISSN)
대한독성유전 단백체학회 (The Korean Society of Toxicogenomics and Toxicoproteomics)
권호 표지

Iron Can Accelerate the Conjugation Reaction between Abeta 1-40 Peptide and MDA

  • Park, Yong-Hoon (Inam Neuroscience Research Center, San bon Medical Center, Wonkwang University) ;
  • Jung, Jai-Yun (Department of Anesthesiology and Pain Medicine, San bon Medical Center, Wonkwang University) ;
  • Son, Il-Hong (Inam Neuroscience Research Center, San bon Medical Center, Wonkwang University)
  • 발행 : 2009.06.30
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초록

Alzheimer's disease(AD) is a neurodegenerative disorder characterized pathologically by senile plaques, neurofibrillary tangles, and synapse loss. Especially, extracellular beta-amyloid (Abeta) deposition is a major pathological hallmark of Alzheimer's disease (AD). In AD senile plaques, high level of iron and car-bonylated Abeta were detected. Iron has a Lewis acid property which can increase the electrophilicity of carbonyls, which may react catalytically with nucleophiles, such as amines. Hence, this study investigated whether or not iron could promote the carbonylation of amine with malondialdehyde (MDA) in the physiological condition. As the basic study, we examined that iron might promote the conjugation reaction between propylamine, monoamine molecule and MDA in the physiological condition. As the concentration of iron increased, the fluorescence intensity produced from the conjugation reaction increased in a dose-dependent manner. Instead of propylamine, we applied the same reaction condition to Abeta 1-40 peptide, one of major components founded in AD senile plaques for the conjugation reaction. As the result, the fluorescence intensity produced from the conjugation reaction between Abeta 1-40 peptide and MDA showed the similar trend to that of the reaction used with propylamine. This study suggests that iron can accelerate the conjugation reaction of MDA to Abeta 1-40 peptide and play an another important role in deterioration of AD brain.

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