Title of article :
Oxidative modification of a proline-rich gliadin peptide
Author/Authors :
Huang، نويسنده , , Xin and Kanerva، نويسنده , , Pنivi and Salovaara، نويسنده , , Hannu and Loponen، نويسنده , , Jussi and Sontag-Strohm، نويسنده , , Tuula، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2013
Pages :
6
From page :
2011
To page :
2016
Abstract :
Prolamins are proline-rich proteins occurring in cereal grains. Prolamins of wheat, barley and rye, or gluten protein, can cause coeliac disease in individuals not tolerating gluten. Degrading harmful prolamins can reduce their toxicity. A model peptide sequenced in α-gliadin, 33-mer (LQLQPFPQPQLPYPQPQLPYPQPQLPYPQPQPF), was chosen for our study. The metal-catalysed oxidation of 33-mer was studied, instead of enzymatic hydrolysis. Peptide 33-mer was treated in several oxidative systems. Iron-catalysed hydrogen peroxide-induced oxidation showed the greatest modification of 33-mer. Carbonyl groups and dityrosine cross-links were readily formed. At best, the immunological activity of 33-mer was reduced to 18% of its initial level after 24 h of oxidation. Oxidative treatment can be further applied for the modification of cereal prolamin proteins, since it appears to be a potential alternative for reduction of coeliac immunological activities in gluten proteins.
Keywords :
Protein oxidation , gliadin , proline , Fenton reaction , coeliac disease , ELISA , Degradation , Dityrosine
Journal title :
Food Chemistry
Serial Year :
2013
Journal title :
Food Chemistry
Record number :
1973623
Link To Document :
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