ABSTRACT
PURPOSE: To determine the DNA protective effects of a standard coffee beverage in comparison to water consumption. METHODS: The single-blind, randomised controlled study with parallel design included healthy women (n = 50) and men (n = 50) recruited from the general Central European population. The subjects were randomised in a coffee and a control group, with stratification for sex and body mass index. The study comprised two periods of 4 weeks: a preconditioning period, with daily consumption of at least 500 ml water but no coffee, nor tea, nor any other caffeine-containing product. During the subsequent intervention period the coffee group consumed 500 ml of freshly brewed dark roast coffee blend per day, the control group consumed water instead. On the last day of each period, blood was drawn and analysed by comet assay (single-cell gel electrophoresis) to assess the level of DNA damage (strand breakage). RESULTS: At the end of the intervention period the mean level of DNA strand breaks in the coffee group has decreased in comparison to the control group [difference in means 0.23% TI (tail intensity), p = 0.028]. The mean change from baseline (delta value) was - 23% in the coffee group (p = 0.0012). Effects of coffee intake were similar for men and women. During intervention, neither group showed any significant change in body weight or calorie intake. CONCLUSIONS: Our results indicate that regular consumption of a dark roast coffee blend has a beneficial protective effect on human DNA integrity in both, men and women.
Subject(s)
Coffee , DNA Damage/drug effects , Adult , Cooking , Europe , Female , Hot Temperature , Humans , Male , Single-Blind MethodABSTRACT
BACKGROUND: Persons with Down syndrome have increased vulnerability to oxidative stress caused by overexpression of superoxide dismutase, an antioxidant enzyme coded on chromosome 21. Increased oxidative stress may lead to oxidative damage of important macromolecules. We monitored this damage by measuring levels of different biomarkers of oxidative stress (protein carbonyls and 4-hydroxy-2-nonenal), as well as plasma antioxidant capacity, in children with Down syndrome. A total of 20 children with Down syndrome and 18 healthy individuals were recruited for this purpose. METHODS: Plasma protein carbonyls were measured using an ELISA technique, 4-hydroxy-2-nonenal was monitored by HPLC and the antioxidant capacity was evaluated using a ferric reducing ability of plasma (FRAP) assay. RESULTS: We found that children with Down syndrome had significantly elevated levels of protein carbonyls compared to healthy controls (p < 0.01). Levels of 4-hydroxy-2-nonenal and antioxidant capacity were similar in both groups. CONCLUSION: Our results on oxidative damage to proteins confirm the assumption of increased oxidative stress in individuals with Down syndrome.
Subject(s)
Antioxidants/analysis , Down Syndrome/diagnosis , Oxidative Stress/physiology , Aldehydes/blood , Biomarkers/blood , Child , Child, Preschool , Down Syndrome/blood , Enzyme-Linked Immunosorbent Assay , Humans , Protein Carbonylation/physiology , Proteins/analysis , Proteins/chemistry , Superoxide Dismutase/bloodABSTRACT
BACKGROUND: Down syndrome (DS) is a chromosomal abnormality (trisomy 21) leading to mental retardation, to the characteristic change of individual's phenotype and to the pathological features of Alzheimer disease. Patients with DS have elevated ratio of superoxide dismutase to (catalase plus glutathione peroxidase) with respect to controls in all age categories suggesting that oxidative imbalance contributes to the clinical manifestation of accelerated aging. RESULTS: We report that persons with DS have elevated uric acid levels compared with controls, 348.56+/-22.78 versus 284.00+/-20.86 micromol/l (p=0.018). The levels of hypoxanthine and xanthine in DS children (6.35+/-0.31 and 1.02+/-0.23 micromol/l) were significantly lower than in controls (7.83+/-0.59 and 2.43+/-0.66 micromol/l). This result suggests increased conversion of hypoxanthine and xanthine to uric acid with subsequent free radical-dependent oxidation of uric acid to allantoin, mechanisms potentiated by the oxidative stress in DS. Allantoin is a nonenzymatic oxidative product of uric acid in human. In DS individuals, the levels of allantoin were significantly higher than those in healthy controls (18.58+/-2.27 and 14.07+/-1.07 micromol/l, respectively, p=0.03). CONCLUSIONS: Our data supported the presumption of increased oxidative stress in DS.
