Carotenoids are part of the human diet and a regular low-dose intake of these compounds from natural sources is normally preferred. Carotenoid supplementation in various diseases, including cancer, was described to be useful, but evidence has been obtained that high-dose supplementation of β-carotene may be unsafe, especially to smokers and asbestos-exposed workers, because of a stastically detected increased cancer risk. The negative effect might be mediated by carotenoid breakdown products having a high reactivity towards biomolecules. It has been suggested that these compounds originate from nonenzymatic cleavage of carotenoids by oxidants liberated in large amounts by neutrophils that accumulate in various inflammatory diseases and, in particular, in pulmonary disorders characterized by profound abnormalities in inflammatory pathways, such as those triggered by tobacco smoking. Carotenoid breakdown products, in turn, may affect neutrophil response in different ways that depend on the concentration that is reached by these products in the medium. In vitro studies show that nanomolar and micromolar concentrations of carotenoid derivatives stimulate superoxide production by neutrophils activated by phorbol myristate acetate (PMA), while a slight inhibition is noticed with cells activated by the chemotactic tripeptide N-formyl-Met-Leu-Phe (f-MLP). At higher concentrations, carotenoid breakdown products inhibit superoxide production in the presence of both PMA and f-MLP. [...]
Neutrophils are a major source of reactive oxygen species (ROS). The role of airway mucous on ROS production is unknown. The aim of our study was to investigate the direct influence of bronchoalveolar lavage fluid (BALF) and induced sputum (IS) alone or in combination with chemical/biological stimulus on ROS production in peripheral blood neutrophils during chronic obstructive pulmonary disease (COPD). Neutrophils were isolated from peripheral blood of 47 patients with moderate COPD and 14 healthy individuals (HI). BALF/RPMI (1:1) or IS/RPMI (1:1) from COPD patients were used to stimulate neutrophils alone or in combination with phorbolmyristate- acetate (PMA) (0.1–30 nM) or Staphylococcus aureus bacteria (0.7–500 bact/neutrophil). Relative generation of ROS was measured flow cytometrically. BALF/RPMI and in combination with relatively low PMA or all bacteria concentrations stimulated ROS; while, combination with relatively high PMA concentrations suppressed ROS in of COPD patients and HI. IS/RPMI and its combination with PMA inhibited ROS generation in both groups; whereas, IS stimulated or had a tendency to stimulate ROS production with relatively high bacteria concentrations. In conclusion, BALF and IS directly or in combination with chemical/biological factors modulated ROS production. This effect was stronger in neutrophils from COPD patients and depended on chemical/biological stimulus intensity.
Vitamin C (ascorbic acid) is an essential water-soluble nutrient that primarily exerts its effect on a host defense mechanisms and immune homeostasis and is the most important physiological antioxidant. Stable intake of vitamin C is essential for life in humans because the body does not synthesize it. Even the numerous studies have demonstrated that vitamin C supplementation stimulates the immune system, prevents DNA damage and significantly decreases the risk of a wide range of pathologies; the potential protective mechanisms are still largely unknown. This review summarizes the recently known facts about the role of vitamin C on the selected cells of the immune system and potential molecular mechanisms involved. Further, in this review, many new data about the positive effects of vitamin C on the immune system, potential toxicological effects, vitamin C supplementation in disease development, as well as some proposed mechanisms of vitamin C activity, are discussed.
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