In vivo, RESV has been shown to increase plasma an tiox idant capacity and decrease lipid peroxidation. Moreover, in spontaneously hypertensive rats RESV signif icantly reduces markersof oxidative stress such as hydroxyguanosine in urine. Likew ise, in guineapigs RESV induces catalase activity in card iac tissue and decreases the concentration of reactive oxygen species. These results indicate that resveratrol can suppress pathological increases in the peroxidation of lipids andother macromo lecules in vivo, and also that these effects are direct, or the result of upregulating endogenous antioxidant enzymes. Current research is therefore focusing on understanding the mechanisms involved in the ab ilityof RESV to increase the activity of sir tuin and the intracellu lar pathways activated or regulated by SIRT.Likew ise, interest in SIRT has also intensified with further discover ies of its involvementin cancer, metabo lic diseases and neurodegenerative disorders, as well as inother fields such as aging med icine, due to its role as a longevity factor in multiple model organisms that have beendivided in to four groups. Their purchase MI-2 products function in a complex as transcrip tional repressors or silencers, acting largely through histone deacety lation. The SIR gene, required for silencing of rDNA loci, is evolutionarily conserved from prokaryotes to humans. Analyses of SIRT enzymatic activ ity has revealed that it functions differently from previouslydescr ibed histone deacety lases. Therefore, SIRT appears to possess two enzymatic activ ities: the deacetylation of a target protein and the metabo lism of NAD. These two activ ities suggest that SIRT could act as a metabolic or oxidative sensor, regulating cellu lar mach inery based on such information. Therefore, it can be hypothesized that the benefits of RESV are due either to its an tiox idant properties or to a specific activation of SIRT, wh ich is involved in responding to molecular damage and metabolic imbalances. Proapoptotic signaling in response to genotoxic stress: DNA doublestrand breaks activate the signal tran sducer ATM.ATM phosphorylation of the transcription factor p leadsto its stabilization and activation,promoting cell cycle arrest and apop tosis.ATM also favours the tran slocation to the cytoplasm, activating IKK, which phosphorylates I B leads to its polyubiquitination and proteo somal degradation, releasing NF B transcription factor, which moves to the nucleusand in response to genotoxic stress increases expression of proapoptotic genes.SIRT deacety lates p and NF B, causing their inactivation and dampening of proapoptotic signals.Hyperactivity of theproapoptotic factor p accelerates ageing and NF. However, the molecular and signalling cascades may differ from cell to cell.The antiproliferative effectsof RESV are associatedwith an inhibition of cell cycle proteins and induction of p in tumour cells; however, in neuronal cells the neuroprotective effects via SIRT activation may be mediated by p inhib ition. Moreover, SIRT also deacety lates nuclear receptor peroxisomeproliferator activated recep tor, which regulates awide range of metabolic activ ities in Targetmol’s Bendamustine hydrochloride muscle, adipose tissues and liver. In the liver, SIRT deacetylases the coactivator PGC, thereby increasing expressionof genes forgluconeogenesis.This enzyme is activated downstream of PIK by recruitment to the plasma membrane through direct contact with phosphatidy linosito l, tr isphosphate, and then phosphorylated by the phosphoinositidedependent proteinkinases PDK and PDK.