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Impact of the carotenoid astaxanthin on phagocytic capacity and ROS/RNS production of human neutrophils treated with free fatty acids and high glucose.
MedLine Citation:
PMID:  22008307     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
BACKGROUND: The purpose of the present study was to evaluate the effect of carotenoid astaxanthin (ASTA) on human neutrophils treated with high glucose and free fatty acids (FFA) on the phagocytic capacity and reactive oxygen/nitrogen species production. METHODS: The following parameters were evaluated: phagocytic capacity of neutrophils by using zymosan particles, intracellular and extracellular superoxide anion (lucigenin and DHE probes), hydrogen peroxide (H(2)O(2) - phenol red), nitric oxide (Griess reagent) production, and maximal activity of G6PDH. RESULTS: There was a decreased phagocytic capacity of human neutrophils treated with high glucose (30mM) or FFA (0.1mM) and a partial restoring of the phagocytic capacity after ASTA-treatment was observed. ROS and RNS production was increased in neutrophils due to both high glucose and FFA. This increase in ROS/RNS production was also partially prevented by ASTA treatment. Both glucose and FFA increased the G6PDH activity. We show that ASTA provides a modest improvement of cellular functions after cells have been treated with high glucose and FFA. CONCLUSIONS: In summary, this study showed that both high glucose and a mixture of FFA are potent inducers of ROS/RNS production on neutrophils as observed by higher levels of superoxide anion, hydrogen peroxide and NO production. Also, these metabolites decrease the phagocytic capacity of neutrophils and increase the G6PDH activity. Overall, ASTA-treatment was able to reduce partially ROS/RNS production by reducing the availability of NADPH and recover phagocytic capacity of neutrophils.
Authors:
Beatriz Alves Guerra; Rosemari Otton
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-10-15
Journal Detail:
Title:  International immunopharmacology     Volume:  -     ISSN:  1878-1705     ISO Abbreviation:  -     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-10-19     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100965259     Medline TA:  Int Immunopharmacol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2011. Published by Elsevier B.V.
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