The steady-state levels of oxidative DNA damage and of lipid peroxidation (F2-isoprostanes) are not correlated in healthy human subjects

2000 ◽  
Vol 32 (4) ◽  
pp. 355-362 ◽  
Author(s):  
Timothy England ◽  
Emily Beatty ◽  
Almas Rehman ◽  
Jaffar Nourooz-Zadeh ◽  
Paulo Pereira ◽  
...  
2000 ◽  
Vol 84 (6) ◽  
pp. 919-925 ◽  
Author(s):  
Emily R. Beatty ◽  
James D. O'Reilly ◽  
Timothy G. England ◽  
Gareth T. McAnlis ◽  
Ian S. Young ◽  
...  

The effect of dietary intake of flavonols (predominantly quercetin) on oxidative DNA damage was studied in thirty-six healthy human subjects (sixteen men, twenty women). The study was a randomised crossover study, comprising two 14 d treatments of either a low-flavonol (LF) or high-flavonol (HF) diet with a 14 d wash-out period between treatments. Subjects were asked to avoid foods containing flavonols, flavones and flavanols during the LF dietary treatment period and to consume one 150 g onion (Allium cepa) cake (containing 89·7 mg quercetin) and one 300 ml cup of black tea (containing 1·4 mg quercetin) daily during the HF dietary treatment. A 7 d food diary was kept during each dietary period and blood samples were taken after each dietary treatment. Products of oxidative damage to DNA bases were measured in DNA from leucocytes. The study had more than 95 % power to detect a change of 20 % in DNA damage products Plasma vitamin C and plasma quercetin concentrations were also measured. No significant differences in intake of macronutrients or assessed micronutrients, measured DNA base damage products, or plasma vitamin C were found between the HF and LF dietary treatments. The plasma quercetin concentration was significantly higher after the HF dietary treatment period (228·5 (SEM 34·7) nmol/l) than after the LF dietary treatment period (less than the limit of detection, i.e. <66·2 nmol/l). These findings do not support the hypothesis that dietary quercetin intake substantially affects oxidative DNA damage in leucocytes.


2011 ◽  
Vol 108 (2) ◽  
pp. 315-326 ◽  
Author(s):  
Inger Ottestad ◽  
Gjermund Vogt ◽  
Kjetil Retterstøl ◽  
Mari C. Myhrstad ◽  
John-Erik Haugen ◽  
...  

Intake of fish oil reduces the risk of CHD and CHD deaths. Marine n-3 fatty acids (FA) are susceptible to oxidation, but to our knowledge, the health effects of intake of oxidised fish oil have not previously been investigated in human subjects. The aim of the present study was to investigate markers of oxidative stress, lipid peroxidation and inflammation, and the level of plasma n-3 FA after intake of oxidised fish oil. In a double-blinded randomised controlled study, healthy subjects (aged 18–50 years, n 54) were assigned into one of three groups receiving capsules containing either 8 g/d of fish oil (1·6 g/d EPA+DHA; n 17), 8 g/d of oxidised fish oil (1·6 g/d EPA+DHA; n 18) or 8 g/d of high-oleic sunflower oil (n 19). Fasting blood and morning spot urine samples were collected at weeks 0, 3 and 7. No significant changes between the different groups were observed with regard to urinary 8-iso-PGF2α; plasma levels of 4-hydroxy-2-hexenal, 4-hydroxy-2-nonenal and α-tocopherol; serum high sensitive C-reactive protein; or activity of antioxidant enzymes in erythrocytes. A significant increase in plasma level of EPA+DHA was observed in both fish oil groups, but no significant difference was observed between the fish oil groups. No changes in a variety of in vivo markers of oxidative stress, lipid peroxidation or inflammation were observed after daily intake of oxidised fish oil for 3 or 7 weeks, indicating that intake of oxidised fish oil may not have unfavourable short-term effects in healthy human subjects.


2010 ◽  
Vol 49 (7) ◽  
pp. 449-454 ◽  
Author(s):  
Charles la Porte ◽  
Nha Voduc ◽  
Guijun Zhang ◽  
Isabelle Seguin ◽  
Danielle Tardiff ◽  
...  

Author(s):  
Buqing Yi ◽  
Igor Nichiporuk ◽  
Matthias Feuerecker ◽  
Gustav Schelling ◽  
Alexander Chouker

2020 ◽  
Author(s):  
Bin Wang ◽  
Weihong Qiu ◽  
Shijie Yang ◽  
Limin Cao ◽  
Chunmei Zhu ◽  
...  

<a><b>OBJECTIVE: </b></a>Acrylamide exposure from daily-consumed food has raised global concern.<b> </b>We aimed to assess the exposure-response relationships of internal acrylamide exposure with oxidative DNA damage, lipid peroxidation and fasting plasma glucose (FPG) alteration, and investigate the mediating role of oxidative DNA damage and lipid peroxidation in the association of internal acrylamide exposure with FPG. <p><b>RESEARCH DESIGN AND METHODS:</b> FPG and urinary biomarkers of oxidative DNA damage (8-hydroxy-deoxy-guanosine, 8-OHdG), lipid peroxidation (8-iso-prostaglandin-F2α, 8-iso-PGF2α) and acrylamide exposure (N-acetyl-S-(2-carbamoylethyl)-L-cysteine, AAMA; N-acetyl-S-(2-carbamoyl-2-hydroxyethyl)-L-cysteine, GAMA) were measured for 3,270 general adults from the Wuhan-Zhuhai cohort. The associations of urinary acrylamide metabolites with 8-OHdG, 8-iso-PGF2α and FPG were assessed by linear mixed models. The mediating roles of 8-OHdG and 8-iso-PGF2α were evaluated by mediation analysis.</p> <p><b>RESULTS:</b> We found significant linear positive dose-response relationships of urinary acrylamide metabolites with 8-OHdG, 8-iso-PGF2α and FPG (except GAMA with FPG), and 8-iso-PGF2α with FPG. Each 1-unit increase in log-transformed level of AAMA, ΣUAAM (AAMA+GAMA) or 8-iso-PGF2α was associated with a 0.17-, 0.15- or 0.23-mmol/L increase in FPG, respectively (<i>P </i>or/and<i> P trend</i><0.05). Each 1% increase in AAMA, GAMA or ΣUAAM was associated with a 0.19%, 0.27% or 0.22% increase in 8-OHdG, respectively, and a 0.40%, 0.48% or 0.44% increase in 8-iso-PGF2α, respectively (<i>P </i>and<i> P trend</i><0.05). Increased 8-iso-PGF2α rather than 8-OHdG significantly mediated 64.29% and 76.92% of the AAMA and ΣUAAM associated-FPG increases, respectively.</p> <p><b>CONCLUSIONS:</b> Exposure of general adult population to acrylamide was associated with FPG elevation, oxidative DNA damage and lipid peroxidation, which in turn partly mediated acrylamide-associated FPG elevation.<b></b></p>


Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 618
Author(s):  
Riley Larson ◽  
Courtney Nelson ◽  
Renee Korczak ◽  
Holly Willis ◽  
Jennifer Erickson ◽  
...  

Acacia gum (AG) is a non-viscous soluble fiber that is easily incorporated into beverages and foods. To determine its physiological effects in healthy human subjects, we fed 0, 20, and 40 g of acacia gum in orange juice along with a bagel and cream cheese after a 12 h fast and compared satiety, glycemic response, gastrointestinal tolerance, and food intake among treatments. Subjects (n = 48) reported less hunger and greater fullness at 15 min (p = 0.019 and 0.003, respectively) and 240 min (p = 0.036 and 0.05, respectively) after breakfast with the 40 g fiber treatment. They also reported being more satisfied at 15 min (p = 0.011) and less hungry with the 40 g fiber treatment at 30 min (p = 0.012). Subjects reported more bloating, flatulence, and GI rumbling on the 40 g fiber treatment compared to control, although values for GI tolerance were all low with AG treatment. No significant differences were found in area under the curve (AUC) or change from baseline for blood glucose response, although actual blood glucose with 20 g fiber at 30 min was significantly less than control. Individuals varied greatly in their postprandial glucose response to all treatments. AG improves satiety response and may lower peak glucose response at certain timepoints, and it is well tolerated in healthy human subjects. AG can be added to beverages and foods in doses that can help meet fiber recommendations.


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