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European Journal of Nutrition 2015-Oct

Effect of polyphenol supplements on redox status of blood cells: a randomized controlled exercise training trial.

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Lucrecia Carrera-Quintanar
Lorena Funes
Nestor Vicente-Salar
Cristina Blasco-Lafarga
Antoni Pons
Vicente Micol
Enrique Roche

Ключевые слова

абстрактный

OBJECTIVE

The effect of endogenous antioxidants can be either an immediate response (relying on enzymatic activities) or a long-term adaptation (relying on gene modulation events), both susceptible to be modified by antioxidants from diet and supplementation. The aim of this work was to delve in these aspects in circulating white blood cells in a group of volunteers (n = 33, 20-22 years) performing eccentric exercises and consuming or not (n = 8) different polyphenolic antioxidants (Lippia citriodora extract-PLX(®) n = 8, almond beverage n = 9 or a mixture of both n = 8) during 21 days.

METHODS

We have designed a single-blind, parallel-group, randomized controlled trial. Antioxidant enzyme activities, oxidative stress markers, and antioxidant gene expression were determined.

RESULTS

Neutrophils and lymphocytes expressed high amounts of oxidative markers compared to plasma. Concerning enzymatic activities, increased superoxide dismutase levels were detected when certain supplements were consumed. However, catalase levels did not change. As for glutathione peroxidase levels, no differences were detected in lymphocytes, while neutrophils expressed increased levels in both placebo and PLX(®) groups. Glutathione reductase activity was decreased in all groups, except in neutrophils of PLX(®) group. At the level of gene expression, neither PLX(®) nor the almond beverage interfered with the expression of genes coding for the corresponding enzymes. However, the combined intake of both supplements affected the expression of glutathione reductase and Cu-Zn and Mn-superoxide dismutases in neutrophils.

CONCLUSIONS

Altogether, these results suggest that blood cell types respond and adapt differently to exercise-induced oxidative damage.

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