Amino Acids

, Volume 43, Issue 1, pp 91–96

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

Authors

  • Konstantin Kulebyakin
    • Department of Biochemistry, School of Biology, Room 141M.V. Lomonosov Moscow State University
  • Larisa Karpova
    • Department of Biochemistry, School of Biology, Room 141M.V. Lomonosov Moscow State University
  • Ekaterina Lakonsteva
    • Chemical Diversity Research Institute
  • Mikhail Krasavin
    • Chemical Diversity Research Institute
    • Department of Biochemistry, School of Biology, Room 141M.V. Lomonosov Moscow State University
    • Research Center of Neurology RAMS
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