The effect of carnosine on methylglyoxal-induced oxidative stress in rats

YıLMAZ Z., Kalaz E. B., Aydın A. F., Soluk-Tekkeşin M., Doğru-Abbasoğlu S., Uysal M. M., ...Daha Fazla

ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY, sa.3, ss.192-198, 2017 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Basım Tarihi: 2017
  • Doi Numarası: 10.1080/13813455.2017.1296468
  • Dergi Adı: ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.192-198
  • Anahtar Kelimeler: Dicarbonyl stress, protein carbonyl, advanced glycation end products, advanced oxidation products of protein, imidazole dipeptide, ADVANCED GLYCATION, END-PRODUCTS, BIOMARKERS, TOXICITY, PROTEINS, PROTECTS, DAMAGE, SERUM
  • İstanbul Üniversitesi Adresli: Evet

Özet

Methylglyoxal (MG) is generated from glycolytic metabolites, lipid peroxidation, glucose autooxidation and protein glycation. It is a prooxidant inducing oxidative stress and formation of advanced glycation end products (AGE). Effect of carnosine (CAR) as an antioxidant on toxicity due to MG has generated interest. In this study, rats were given incrementally increased doses (100-300 mg/kg) of MG in drinking water for ten weeks. CAR (250 mg/kg i.p.) was administered with MG. Plasma thiobarbituric reactive substances (TBARS), protein carbonyl (PC), advanced oxidation protein products (AOPP) and AGE levels were elevated by MG, and CAR decreased PC, AOPP and AGE levels. MG increased liver reactive oxygen species (ROS), TBARS, PC and AOPP levels, which were decreased by CAR. Thus, in vivo role of CAR on chronic MG administration was observed to suppress the generated hepatic and plasma oxidative stress.