Fructose-Induced Carbonyl/Oxidative Stress inS. cerevisiae: Involvement of TOR
| Autor: | Ruslana Vasylkovska, Liudmyla Lozinska, Bohdana V. Valishkevych, Semchyshyn Hm |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
chemistry.chemical_classification Article Subject Cell growth Saccharomyces cerevisiae Fructose Biology medicine.disease_cause biology.organism_classification Biochemistry Yeast Amino acid lcsh:Biochemistry 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology chemistry medicine Monosaccharide lcsh:QD415-436 Signal transduction Oxidative stress Research Article |
| Zdroj: | Biochemistry Research International Biochemistry Research International, Vol 2016 (2016) |
| ISSN: | 2090-2255 2090-2247 |
| DOI: | 10.1155/2016/8917270 |
| Popis: | The TOR (target of rapamycin) signaling pathway first described in the budding yeastSaccharomyces cerevisiaeis highly conserved in eukaryotes effector of cell growth, longevity, and stress response. TOR activation by nitrogen sources, in particular amino acids, is well studied; however its interplay with carbohydrates and carbonyl stress is poorly investigated. Fructose is a more potent glycoxidation agent capable of producing greater amounts of reactive carbonyl (RCS) and oxygen species (ROS) than glucose. The increased RCS/ROS production, as a result of glycoxidationin vivo, is supposed to be involved in carbonyl/oxidative stress, metabolic disorders, and lifespan shortening of eukaryotes. In this work we aim to expand our understanding of how TOR is involved in carbonyl/oxidative stress caused by reducing monosaccharides. It was found that in fructose-grown compared with glucose-grown cells the level of carbonyl/oxidative stress markers was higher. The defects in the TOR pathway inhibited metabolic rate and suppressed generation of glycoxidation products in fructose-grown yeast. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|