Document Detail

Short-term blackcurrant extract consumption modulates exercise-induced oxidative stress and lipopolysaccharide-stimulated inflammatory responses.
MedLine Citation:
PMID:  19403859     Owner:  NLM     Status:  MEDLINE    
Exercise-induced oxidative stress is instrumental in achieving the health benefits from regular exercise. Therefore, inappropriate use of fruit-derived products (commonly applied as prophalytic antioxidants) may counteract the positive effects of exercise. Using human exercise and cellular models we found that 1) blackcurrant supplementation suppressed exercise-induced oxidative stress, e.g., plasma carbonyls (0.9 +/- 0.1 vs. 0.6 +/- 0.1 nmol/mg protein, placebo vs. blackcurrant), and 2) preincubation of THP-1 cells with an anthocyanin-rich blackcurrant extract inhibited LPS-stimulated cytokine secretion [TNF-alpha (16,453 +/- 322 vs. 10,941 +/- 82 pg/ml, control vs. extract, P < 0.05) and IL-6 (476 +/- 14 vs. 326 +/- 32 pg/ml, control vs. extract, P < 0.05)] and NF-kappaB activation. In addition to its antioxidant and anti-inflammatory properties, we found that postexercise plasma collected after blackcurrant supplementation enhanced the differential temporal LPS-stimulated inflammatory response in THP-1 cells, resulting in an early suppression of TNF-alpha (1,741 +/- 32 vs. 1,312 +/- 42 pg/ml, placebo vs. blackcurrant, P < 0.05) and IL-6 (44 +/- 5 vs. 36 +/- 3 pg/ml, placebo vs. blackcurrant, P < 0.05) secretion after 24 h. Furthermore, by using an oxidative stress cell model, we found that preincubation of THP-1 cells with hydrogen peroxide (H(2)O(2)) prior to extract exposure caused a greater suppression of LPS-stimulated cytokine secretion after 24 h, which was not evident when cells were simultaneously incubated with H(2)O(2) and the extract. In summary, our findings support the concept that consumption of blackcurrant anthocyanins alleviate oxidative stress, and may, if given at the appropriate amount and time, complement the ability of exercise to enhance immune responsiveness to potential pathogens.
K A Lyall; S M Hurst; J Cooney; D Jensen; K Lo; R D Hurst; L M Stevenson
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Publication Detail:
Type:  Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-04-29
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  297     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-07-03     Completed Date:  2009-08-25     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R70-81     Citation Subset:  IM    
Health & Food Group, The New Zealand Institute for Plant and Food Research, Ltd., Hamilton. New Zealand.
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MeSH Terms
Anthocyanins / administration & dosage*,  isolation & purification
Anti-Inflammatory Agents / administration & dosage*,  isolation & purification
Antioxidants / administration & dosage*,  isolation & purification
Cell Line
Cross-Over Studies
Dietary Supplements*
Dose-Response Relationship, Drug
Double-Blind Method
Drug Administration Schedule
I-kappa B Proteins / metabolism
Inflammation / immunology,  prevention & control*
Interleukin-6 / blood
Middle Aged
Monocytes / drug effects,  immunology
Oxidative Stress / drug effects*
Plant Extracts / administration & dosage
Protein Carbonylation / drug effects
Reactive Oxygen Species / metabolism
Ribes* / chemistry
Time Factors
Transcription Factor RelA / metabolism
Tumor Necrosis Factor-alpha / blood
Reg. No./Substance:
0/Anthocyanins; 0/Anti-Inflammatory Agents; 0/Antioxidants; 0/I-kappa B Proteins; 0/IL6 protein, human; 0/Interleukin-6; 0/Lipopolysaccharides; 0/Plant Extracts; 0/RELA protein, human; 0/Reactive Oxygen Species; 0/Transcription Factor RelA; 0/Tumor Necrosis Factor-alpha; 0/lipopolysaccharide, Escherichia coli 0111 B4; 139874-52-5/NF-kappaB inhibitor alpha

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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