Title of article
Inhibition of cathepsins and related proteases by amino acid, peptide, and protein hydroperoxides
Author/Authors
Henrietta A. Headlam، نويسنده , , Michelle Gracanin، نويسنده , , Kenneth J. Rodgers، نويسنده , , Michael J. Davies، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2006
Pages
10
From page
1539
To page
1548
Abstract
Reaction of radicals in the presence of O2, and singlet oxygen, with some amino acids, peptides, and proteins yields hydroperoxides. These species are key intermediates in chain reactions and protein damage. Previously we have shown that peptide and protein hydroperoxides react rapidly with thiols, and that this can result in inactivation of thiol-dependent enzymes. The major route for the cellular removal of damaged proteins is via catabolism mediated by proteosomal and lysosomal pathways; cysteine proteases (cathepsins) play a key role in the latter system. We hypothesized that inactivation of cysteine proteases by hydroperoxide-containing oxidised proteins may contribute to the accumulation of modified proteins within cells. We show here that thiol-dependent cathepsins, either isolated or in cell lysates, are rapidly and efficiently inactivated by amino acid, peptide, and protein hydroperoxides in a time- and concentration-dependent manner; this occurs with similar efficacy to equimolar H2O2. Inactivation involves reaction of the hydroperoxide with Cys residues as evidenced by thiol loss and formation of sulfenic acid intermediates. Structurally related, non-thiol-dependent cathepsins are less readily inactivated by these hydroperoxides. This inhibition, by oxidized proteins, of the system designed to remove modified proteins, may contribute to the accumulation of damaged proteins in cells subject to oxidative stress.
Keywords
cathepsin , papain , protein oxidation , Protein hydroperoxides , Thiol oxidation , enzyme inhibition , free radicals
Journal title
Free Radical Biology and Medicine
Serial Year
2006
Journal title
Free Radical Biology and Medicine
Record number
520532
Link To Document