NMR-based metabonomic analysis of HUVEC cells during replicative senescence

, and cellular metabolic profiles were gradually altered. Totally, 8, 16, 21 and 19 significant metabolites were primarily changed in the P6, P10, P14 and P18 cells compared with the P3 cells, respectively. These metabolites were mainly involved in 14 significantly altered metabolic pathways. Furthermore, we observed taurine retarded oxidative damage resulting from senescence. In the case of energy deficiency, HUVECs metabolized neutral amino acids to replenish energy, thus increased glutamine, aspartate and asparagine at the early stages of cellular senescence but decreased them at the later stages. Our results indicate that cellular replicative senescence is closely associated with promoted oxidative stress, impaired energy metabolism and blocked protein synthesis. This work may provide mechanistic understanding of the progression of cellular senescence.