Amino Acids

, Volume 43, Issue 1, pp 91–96

Carnosine protects neurons against oxidative stress and modulates the time profile of MAPK cascade signaling

  • Konstantin Kulebyakin
  • Larisa Karpova
  • Ekaterina Lakonsteva
  • Mikhail Krasavin
  • Alexander Boldyrev
Original Article

DOI: 10.1007/s00726-011-1135-4

Cite this article as:
Kulebyakin, K., Karpova, L., Lakonsteva, E. et al. Amino Acids (2012) 43: 91. doi:10.1007/s00726-011-1135-4

Abstract

Carnosine is a known protector of neuronal cells against oxidative injury which prevents both apoptotic and necrotic cellular death. It was shown earlier that carnosine serves as an intracellular buffer of free radicals. Using the model of ligand-dependent oxidative stress in neurons, we have shown that homocysteine (HC) initiates long-term activation of extracellular signal regulated kinase, isoforms 1 and 2 (ERK 1/2) and Jun N-terminal kinase (JNK) which corresponds to exitotoxic effect resulting in cellular death. l-Carnosine (β-alanyl-l-histidine) protects neurons from both excitotoxic effect of homocysteine and cellular death. Its analogs, β-alanyl-d-histidine (d-carnosine) and l-histidyl-β-alanine, restricted accumulation of free radicals and delayed activation of ERK1/2 and JNK in neuronal cells, but did not promote neuronal viability.

Keywords

HyperhomocysteinemiaCarnosineExcitotoxicityMAPKNeuroprotection

Copyright information

© Springer-Verlag 2011

Authors and Affiliations

  • Konstantin Kulebyakin
    • 1
  • Larisa Karpova
    • 1
  • Ekaterina Lakonsteva
    • 2
  • Mikhail Krasavin
    • 2
  • Alexander Boldyrev
    • 1
    • 3
  1. 1.Department of Biochemistry, School of Biology, Room 141M.V. Lomonosov Moscow State UniversityMoscowRussia
  2. 2.Chemical Diversity Research InstituteMoscow RegionRussia
  3. 3.Research Center of Neurology RAMSMoscowRussia