![]() ![]() ![]() In addition, TOR, as a central controller of cell growth, may respond to different types of stress and plays an important role under stressful conditions other than nutrient limitation. Most studies on TOR activation by nutrients were focused on nitrogen sources, while carbohydrates have received less attention. For example, TOR promotes cell growth in response to nutrient availability. ![]() It is well documented that signaling through the TOR pathway is activated by various extracellular and intracellular challenges when conditions are favorable for growth. For instance, the excessive fructose intake in animals has been demonstrated to cause carbonyl/oxidative stress. The detrimental effects of long-term application of fructose in different experimental models can be explained by high level of glycoxidation products. At the same time, fructose, the intake of which increased considerably during the past several decades, is suggested to be more extensively than glucose involved in nonenzymatic processes and generation of reactive species. Glucose is the least reactive reducing monosaccharide, and this characteristic is considered to be responsible for the emergence of glucose as the primary metabolic fuel. Among the mechanisms thought to be responsible for metabolic disturbances, increased ROS/RCS production, as a result of glycoxidation, is the most well supported one. IntroductionĪ strong positive correlation between the intake of excessive dietary carbohydrates and metabolic disorders has been observed in many experimental and clinical studies. The defects in the TOR pathway inhibited metabolic rate and suppressed generation of glycoxidation products in fructose-grown yeast. It was found that in fructose-grown compared with glucose-grown cells the level of carbonyl/oxidative stress markers was higher. In this work we aim to expand our understanding of how TOR is involved in carbonyl/oxidative stress caused by reducing monosaccharides. The increased RCS/ROS production, as a result of glycoxidation in vivo, is supposed to be involved in carbonyl/oxidative stress, metabolic disorders, and lifespan shortening of eukaryotes. Fructose is a more potent glycoxidation agent capable of producing greater amounts of reactive carbonyl (RCS) and oxygen species (ROS) than glucose. TOR activation by nitrogen sources, in particular amino acids, is well studied however its interplay with carbohydrates and carbonyl stress is poorly investigated. The TOR (target of rapamycin) signaling pathway first described in the budding yeast Saccharomyces cerevisiae is highly conserved in eukaryotes effector of cell growth, longevity, and stress response. ![]()
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