Macrophages superoxide release

Berg I, Schulter T, Gercken G. Increase of bovine alveolar macrophage superoxide anion and hydrogen peroxide release by dusts of different origin. J Toxicol Environ Health 1993 39 241-354. 

Colepicolo, P., et al. (1990). A sensitive and specific assay for superoxide anion released by neutrophils or macrophages based on bioluminescence of polynoidin. Anal. Biochem. 184 369-374. 

Damon, M., Cluzel, M., Chanez, P. and Goddard, P. (1989). Phagocytosis induction of chemiluminescence and chemoattractant-increased superoxide anion release from activated human alveolar macrophages in asthma. J. Biolumin. Chemolumin. 4, 279-286. 

To study the effects of iron overloading on inflammatory cells, Muntane et al. [186] investigated the effect of iron dcxtran administration on the acute and chronic phases of carrageenan-induced glanuloma. It was found that iron dcxtran increased the iron content in plasma and stores, and enhanced lipid peroxidation and superoxide production by inflammatory cells. At the same time, iron dcxtran had a beneficial effect on recovery from the anemia of inflammation. It has been suggested that iron overload may affect nitric oxide production in animals. For example, alveolar macrophages from iron-overloaded rats stimulated with LPS or interferon-7 diminished NO release compared to normal rats [187]. 

High antioxidative activity carvedilol has been shown in isolated rat heart mitochondria [297] and in the protection against myocardial injury in postischemic rat hearts [281]. Carvedilol also preserved tissue GSL content and diminished peroxynitrite-induced tissue injury in hypercholesterolemic rabbits [298]. Habon et al. [299] showed that carvedilol significantly decreased the ischemia-reperfusion-stimulated free radical formation and lipid peroxidation in rat hearts. Very small I50 values have been obtained for the metabolite of carvedilol SB 211475 in the iron-ascorbate-initiated lipid peroxidation of brain homogenate (0.28 pmol D1), mouse macrophage-stimulated LDL oxidation (0.043 pmol I 1), the hydroxyl-initiated lipid peroxidation of bovine pulmonary artery endothelial cells (0.15 pmol U1), the cell damage measured by LDL release (0.16 pmol l-1), and the promotion of cell survival (0.13 pmol l-1) [300]. SB 211475 also inhibited superoxide production by PMA-stimulated human neutrophils. 

Pulmonary macrophages cultured in vitro for 20 h with media containing 14.5-58.0 mg Ni/kg as nickel chloride Concentration-dependent decrease in viability of alveolar macrophages highest dose had survival of <50%. Death associated with release of superoxide anions 11... 

Results from several studies suggest that Pb exposure of macrophages can increase the release of superoxide anion and/or hydrogen peroxide, at least shortly after exposure. 

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