Aging
Navigate
Review|Volume 10, Issue 5|pp 868—901

Origin and pathophysiology of protein carbonylation, nitration and chlorination in age-related brain diseases and aging

Efstathios S. Gonos1, Marianna Kapetanou1,2, Jolanta Sereikaite3, Grzegorz Bartosz4, Katarzyna Naparło5, Michalina Grzesik5, Izabela Sadowska-Bartosz5
  • 1National Hellenic Research Foundation, Institute of Biology, Medicinal Chemistry and Biotechnology, Athens 11635 , Greece
  • 2Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Athens, Athens 15701, Greece
  • 3Department of Chemistry and Bioengineering, Faculty of Fundamental Sciences, Vilnius Gediminas Technical University, Vilnius 2040, Lithuania
  • 4Department of Molecular Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, Lodz 90-236, Poland
  • 5Department of Analytical Biochemistry, Faculty of Biology and Agriculture, University of Rzeszow, Rzeszow 35-601, Poland
Received: April 9, 2018Accepted: May 8, 2018Published: May 17, 2018

Copyright: © 2018 Gonos et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Non-enzymatic protein modifications occur inevitably in all living systems. Products of such modifications accumulate during aging of cells and organisms and may contribute to their age-related functional deterioration. This review presents the formation of irreversible protein modifications such as carbonylation, nitration and chlorination, modifications by 4-hydroxynonenal, removal of modified proteins and accumulation of these protein modifications during aging of humans and model organisms, and their enhanced accumulation in age-related brain diseases.