Original Article

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 KulebyakinAffiliated withDepartment of Biochemistry, School of Biology, Room 141, M.V. Lomonosov Moscow State University
  • , Larisa KarpovaAffiliated withDepartment of Biochemistry, School of Biology, Room 141, M.V. Lomonosov Moscow State University
  • , Ekaterina LakonstevaAffiliated withChemical Diversity Research Institute
  • , Mikhail KrasavinAffiliated withChemical Diversity Research Institute
  • , Alexander BoldyrevAffiliated withDepartment of Biochemistry, School of Biology, Room 141, M.V. Lomonosov Moscow State UniversityResearch Center of Neurology RAMS Email author 

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access

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

Hyperhomocysteinemia Carnosine Excitotoxicity MAPK Neuroprotection