Impact of the carotenoid astaxanthin on phagocytic capacity and ROS/RNS production of human neutrophils treated with free fatty acids and high glucose

BackgroundThe 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.MethodsThe following parameters were evaluated: phagocytic capacity of neutrophils by using zymosan particles, intracellular and extracellular superoxide anion (lucigenin and DHE probes), hydrogen peroxide (H2O2 - phenol red), nitric oxide (Griess reagent) production, and maximal activity of G6PDH.ResultsThere was a decreased phagocytic capacity of human neutrophils treated with high glucose (30 mM) or FFA (0.1 mM) 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.ConclusionsIn 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.

► Effect of ASTA on neutrophils treated with high glucose and FFA on the phagocytic capacity and ROS/RNS production. ► High glucose and FFA increased ROS production and decreased phagocytic capacity. ► ASTA partially prevent ROS production induced by FFA and high glucose and recover phagocytic capacity.