Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2006
Effect of sodium sulfite on mast cell degranulation and oxidant stress.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Collaco Christopher R, Hochman Daniel J, Goldblum Randall M, Brooks Edward G
Аннотация
BACKGROUND: Sulfur dioxide is 1 of 6 environmental pollutants monitored by the Environmental Protection Agency. Its ability to induce bronchoconstriction is well documented. It is highly soluble, initially forming sulfite ions in solution. Sulfur oxides are important constituents of other pollutants, such as diesel exhaust and fine particulates.
OBJECTIVE: To investigate the cellular responses of sulfite on cultured mast cells (rat basophilic leukemia [RBL-2H3] cells) and human peripheral blood basophils.
METHODS: Sulfite-induced mast cell degranulation and intracellular production of reactive oxygen species were evaluated in the presence and absence of antioxidants and inhibitors of redox metabolism. Degranulation was determined using beta-hexosaminidase, serotonin, and histamine release assays. Induction of intracellular reactive oxygen species generation was determined using the redox-sensitive dye 2',7'-dichlorofluorescein diacetate.
RESULTS: Sodium sulfite induced degranulation and the generation of intracellular reactive oxygen species in RBL-2H3 cells. These responses were inhibited by the free radical scavenger tetramethylthiourea and the flavoenzyme inhibitor diphenyliodinium but not by depletion of extracellular calcium. Peripheral blood basophils also showed histamine release after exposure to sodium sulfite
CONCLUSIONS: Sulfite, the aqueous ion of sulfur dioxide, induces cellular activation, leading to degranulation in mast cells through a non-IgE-dependent pathway. The response also differs from IgE-mediated degranulation in that it is insensitive to the influx of extracellular calcium. The putative pathway seems to rely on activation of the reduced form of nicotinamide adenine dinucleotide phosphate oxidase complex, leading to intracellular oxidative stress.
OBJECTIVE: To investigate the cellular responses of sulfite on cultured mast cells (rat basophilic leukemia [RBL-2H3] cells) and human peripheral blood basophils.
METHODS: Sulfite-induced mast cell degranulation and intracellular production of reactive oxygen species were evaluated in the presence and absence of antioxidants and inhibitors of redox metabolism. Degranulation was determined using beta-hexosaminidase, serotonin, and histamine release assays. Induction of intracellular reactive oxygen species generation was determined using the redox-sensitive dye 2',7'-dichlorofluorescein diacetate.
RESULTS: Sodium sulfite induced degranulation and the generation of intracellular reactive oxygen species in RBL-2H3 cells. These responses were inhibited by the free radical scavenger tetramethylthiourea and the flavoenzyme inhibitor diphenyliodinium but not by depletion of extracellular calcium. Peripheral blood basophils also showed histamine release after exposure to sodium sulfite
CONCLUSIONS: Sulfite, the aqueous ion of sulfur dioxide, induces cellular activation, leading to degranulation in mast cells through a non-IgE-dependent pathway. The response also differs from IgE-mediated degranulation in that it is insensitive to the influx of extracellular calcium. The putative pathway seems to rely on activation of the reduced form of nicotinamide adenine dinucleotide phosphate oxidase complex, leading to intracellular oxidative stress.