This investigation focused on the qualitative and quantitative composition of polyphenolic compounds of Mediterranean northern shore Cistus creticus and six further, partly sympatric Cistus species (C. albidus, C. crispus, C. ladanifer, C. monspeliensis, C. parviflorus, C. salviifolius). Aqueous extracts of 1153 individual plants from 13 countries were analyzed via high performance liquid chromatography (HPLC). The extracts of C. creticus were primarily composed of two ellagitannins (punicalagin and punicalagin gallate) and nine flavonol glycosides (myricetin and quercetin glycosides, with m-3-O-rhamnoside as the dominant main compound). Differences in the proportions of punicalagin derivatives and flavonol glycosides allowed the classification into two chemovariants. Plants containing punicalagin derivatives and flavonol glycosides were especially abundant in the western and central Mediterranean areas and in Cyprus. From Albania eastwards, punicalagin and punicalagin gallate were of much lesser importance and the predominant chemovariant there was a nearly pure flavonol type. With its two chemovariants, C. creticus takes a central position between the flavonol-rich, purple-flowered clade (besides C. creticus, here represented by C. albidus and C. crispus) and the more ellagitannin-rich, white- or whitish-pink-flowered clade (here represented by C. ladanifer, C. monspeliensis, C. parviflorus and C. salviifolius). The median antioxidative capacity of C. creticus plant material was, with 166 mg Trolox equivalents/g dry wt, about half of the antioxidative capacity of C. ladanifer (301 mg te/g dry wt), the species with the highest antioxidative potential.

Older adults lack of proper physical activity which is often accompanied by vitamin D deficiency. Those factors are known to contribute to health issues in the later years of life. The main goal of this intervention study was to investigate the effect of different vitamin D supplementation strategies for 4 weeks solely or combined with a 10-week strength training program on chromosomal stability in peripheral blood mononuclear cells in community-dwelling older people. One hundred women and men (65-85 years) received either vitamin D3 daily (800 IU), a monthly dose (50.000 IU) or placebo for 17 weeks. All groups received 400 mg calcium daily. The fitness status of the study participants was measured using the 30- second chair stand test, the handgrip strength test and the 6-min walk test. The cytokinesis block micronucleus cytome (CBMN) assay was applied to analyze chromosomal anomalies, including cytotoxic and genotoxic parameters. Changes in antioxidant markers were measured in plasma. Walking distance and chair stand performance improved significantly. Increased levels of the parameters of the CBMN assay were detected for all intervention groups at study end. At baseline micronuclei (MNi) frequency correlated significantly with BMI in both sexes (females: r = 0.369, p = 0.034; males: r = 0.265, p = 0.035), but not with vitamin D serum levels. In females, body fat (r = 0.372, p < 0.001) and functional parameter using the 30-s chair stand test (r = 0.311, p = 0.002) correlated significantly with MNi frequency. Interestingly, not vitamin D supplementation but 10 weeks of resistance training increased MNi frequency indicating elevated chromosomal instability and also adverse effects on antioxidant markers including glutathione and FRAP were detected in the group of community-dwelling older adults.

COVID-19 infections are accompanied by adverse changes in inflammatory pathways that are also partly influenced by increased oxidative stress and might result in elevated DNA damage. The aim of this case-control study was to examine whether COVID-19 patients show differences in oxidative stress-related markers, unconjugated bilirubin (UCB), an inflammation panel and DNA damage compared to healthy, age-and sex-matched controls. The Comet assay with and without the treatment of formamidopyrimidine DNA glycosylase (FPG) and H₂O₂ challenge was used to detect DNA damage in whole blood. qPCR was applied for gene expression, UCB was analyzed via HPLC, targeted proteomics were applied using Olink® inflammation panel and various oxidative stress as well as clinical biochemistry markers were analyzed in plasma. Hospitalized COVID-19 patients (n = 48) demonstrated higher serum levels of 55 inflammatory proteins (p < 0.001), including hs-C-reactive protein levels (p < 0.05), compared to healthy controls (n = 48). Interestingly, significantly increased age-related DNA damage (%-DNA in tail) after formamidopyrimidine DNA glycosylase (FPG) treatment was measured in younger (n = 24, average age 55.7 years; p < 0.05) but not in older COVID-19 patients (n = 24, average age 83.5 years; p > 0.05). Although various oxidative stress markers were not altered (e.g., FRAP, malondialdehyde, p > 0.05), a significant increased ratio of oxidized to reduced glutathione was detected in COVID-19 patients compared to healthy controls (p < 0.05). UCB levels were significantly lower in individuals with COVID-19, especially in younger COVID-19 patients (p < 0.05). These results suggest that COVID-19 infections exert effects on DNA damage related to age in hospitalized COVID-19 patients that might be driven by changes in inflammatory pathways but are not altered by oxidative stress parameters.

A high protein intake at old age is important for muscle protein synthesis, however, this could also trigger protein oxidation with the potential risk for DNA damage. The aim of this study was to investigate whether an increased protein intake at recommended level or well above would affect DNA damage or change levels of reduced (GSH) and oxidised glutathione (GSSG) in community-dwelling elderly subjects. These analyses were performed in two randomized intervention studies, in Austria and in New Zealand. In both randomized control trials, the mean protein intake was increased with whole foods, in the New Zealand study (n = 29 males, 74.2 ± 3.6 years) to 1.7 g/kg body weight/d (10 weeks intervention; p < 0.001)) in the Austrian study (n = 119 males and females, 72.9 ± 4.8 years) to 1.54 g/kg body weight/d (6 weeks intervention; p < 0.001)). In both studies, single and double strand breaks and as formamidopyrimidine—DNA glycosylase-sensitive sites were investigated in peripheral blood mononuclear cells or whole blood. Further, resistance to H₂O₂ induced DNA damage, GSH, GSSG and CRP were measured. Increased dietary protein intake did not impact on DNA damage markers and GSH/GSSG levels. A seasonal-based time effect (p < 0.05), which led to a decrease in DNA damage and GSH was observed in the Austrian study. Therefore, increasing the protein intake to more than 20% of the total energy intake in community-dwelling seniors in Austria and New Zealand did not increase measures of DNA damage, change glutathione status or elevate plasma CRP.

A long, healthy and pain-free life is the goal of an aging society. However, people become increasingly less active in old age, which can lead to sarcopenia. To counteract this development, strength training and a sufficient protein supply are essential. To investigate the effects of a high-protein diet in combination with strength training on oxidative stress markers in older adults, 116 men and women underwent a 17-week single-blind randomized control trial with 3 groups (Control CON, Recommended Protein RP and High Protein HP) as part of the NutriAging Study. After finishing a 6-week dietary intervention, a strength training program was additionally implemented for RP and HP for the remaining study period. CON continued with their habitual protein intake throughout the study. Blood was drawn at three time points (baseline T1, week 8 T2, and after study completion T3) and analyzed for chemical blood parameters and the oxidative stress markers superoxide dismutase (SOD), glutathione-peroxidase (GSH-Px), catalase (CAT), ferric reducing ability potential (FRAP); γ-glutamyl-cysteinyl-glycine (GSH), glutathione disulfide (GSSG), unconjugated bilirubin (UCB), and malondialdehyde (MDA). The results showed a significant time effect of certain blood parameters and all measured oxidative stress markers independent of group allocation. This can be explained by seasonal changes over the study period. Urea and blood urea nitrogen (BUN) were significantly increased in HP, which could be attributed to the high protein intake, however they remained in the normal range. UCB and FRAP were significantly lower in HP, which could be due to the metabolization of the additional protein. Women in particular showed more altered oxidative stress markers as well as reduced uric acid (UA) in the HP group, suggesting lower estrogen secretion during menopause, possibly due to decreased nuclear factor erythroid 2-related factor 2 (NrF2) synthesis and subsequently impaired antioxidant defense. The strength training intervention alone showed no negative effects on blood or oxidative stress parameters. In summary, a high-protein diet along with strength training showed no major impact on oxidative stress in older adults.

Background: Generating oxidative stress in a predictable and controllable way without the risk of causing harm is important for enabling the safe validation of interventions such as dietary polyphenols and ensuring ethical standards in human studies, while also advancing mechanisms involved in the induced oxidative stress. Although, many experimental animal and in vitro models have been developed to conduct oxidative stress-based research, to date, very few reliable human models are available. Objective: This study’s main objective was to establish a standardised exercise model to induce oxidative stress in a repeatable and controllable manner and was tested with dietary polyphenols. Method: We applied a single blinded, randomised, cross-over, placebo-controlled trial with adult (25.95 ± 6.25 years) males (N = 40) where the induction of oxidative stress was achieved by an incremental aerobic exercise activity followed by a maximal anaerobic activity until exhaustion. To assess the model, rooibos polyphenolics was used as one of the interventions, while markers of safety and oxidative stress were measured on various occasions during the trial period. Results: The exercise regime reliably and repeatably induced oxidative stress, evidenced by increased levels of oxidative damage markers, i.e., oxidised glutathione (p = 0.003), malondialdehyde (p = 0.004), and a Comet assay tail moment (p < 0.05), while unconjugated bilirubin (p = 0.002) and the ferric reducing antioxidant potential (p < 0.001) increased over the study period, in the male study participants, irrespective of the oral intervention. Conclusions: This model showed an exercise regime that could be adapted to induce oxidative stress in a reliable and repeatable fashion without risk of causing harm. This study also demonstrated that a dietary polyphenolic intervention with rooibos did not complicate the onset of oxidative stress.