Mediterranean diet supplemented with coenzyme Q10 induces postprandial changes in p53 in response to oxidative DNA damage in elderly subjects

Abstract

Coenzyme Q10 (CoQ) is a powerful antioxidant that reduces oxidative stress. We explored whether the quality of dietary fat alters postprandial oxidative DNA damage and whether supplementation with CoQ improves antioxidant capacity by modifying the activation/stabilization of p53 in elderly subjects. In this crossover study, 20 subjects were randomly assigned to receive three isocaloric diets during 4 weeks each: (1) Mediterranean diet (Med diet), (2) Mediterranean diet supplemented with CoQ (Med+CoQ diet), and (3) saturated fatty acid-rich diet (SFA diet). Levels of mRNAs were determined for p53, p21, p53R2, and mdm2. Protein levels of p53, phosphorylated p53 (Ser20), and monoubiquitinated p53 were also measured, both in cytoplasm and nucleus. The extent of DNA damage was measured as plasma 8-OHdG. SFA diet displayed higher postprandial 8-OHdG concentrations, p53 mRNA and monoubiquitinated p53, and lower postprandial Mdm2 mRNA levels compared with Med and Med +CoQ diets (p<0.05). Moreover, Med+CoQ diet induced a postprandial decrease of cytoplasmatic AGE (2012) 34:389-403

Postprandial changes in the proteome are modulated by dietary fat in patients with metabolic syndrome

“…Previous studies from our laboratory have shown that an HMUFA meal following a long-term consumption of a MUFA-rich diet lowered several postprandial oxidative stress biomarkers as compared to that evoked by an HSFA meal after long-term consumption of an SFA-rich diet [29]. Taking into account that p53 has antioxidant functions protecting the genome from oxidation produced by oxidative stress [30,31], our results suggest that p53 activation by postprandial oxidative stress after an HSFA meal intake -probably by DNA damage, as shown previously in an elderly population [32] -could be responsible for HSPA1A down-regulation and, for the opposite effect, up-regulation after an HMUFA meal, which may be accounted for by a lack of p53 postprandial activation.…”

Postprandial antioxidant gene expression is modified by Mediterranean diet supplemented with coenzyme Q10 in elderly men and women

“…In the same population of this study, we previously demonstrated that the Med diet improves the postprandial oxidative stress with a higher increase in capillary flow and plasma nitric oxide levels, a lower plasma lipid peroxidation products, nitrotyrosine and protein carbonyl levels, lower plasma antioxidant enzyme activities (GPx, catalase (CAT) and SOD), (Yubero-Serrano et al 2010) and lower DNA damage in PBMCs (Gutierrez-Mariscal et al 2011). Addition of exogenous CoQ in synergy with a Med diet had an additive effect reducing the postprandial oxidative stress in elderly men and women.…”

Coenzyme Q10 Rescues Ethanol-induced Corneal Fibroblast Apoptosis through the Inhibition of Caspase-2 Activation

“…CoQ 10 Blocks Caspase-2-mediated EtOH-induced ApoptosisCoQ 10 acts as an anti-apoptotic factor that blocks death signals, including those from EtOH (29,33,35,54). To investigate the relation between the CoQ 10 and caspase-2 activity during EtOH-induced apoptosis, we pretreated the cells with CoQ 10 .…”

“…There is strong evidence that suggests ethanol (EtOH) treatment facilitates the mitochondrial dysfunction (30 -32). Interestingly, CoQ 10 supplements decreased p53-dependent cell death in response to oxidative DNA damage in elderly patients (33).…”