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亚硫酸钠对肥大细胞脱颗粒和氧化应激的影响。

Effect of sodium sulfite on mast cell degranulation and oxidant stress.

作者信息

Collaco Christopher R, Hochman Daniel J, Goldblum Randall M, Brooks Edward G

机构信息

Department of Pediatrics, The University of Texas Medical Branch, Galveston, USA.

出版信息

Ann Allergy Asthma Immunol. 2006 Apr;96(4):550-6. doi: 10.1016/S1081-1206(10)63549-1.

DOI:10.1016/S1081-1206(10)63549-1
PMID:16680925
Abstract

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.

摘要

背景

二氧化硫是美国环境保护局监测的6种环境污染物之一。其诱发支气管收缩的能力已有充分记录。它极易溶于水,最初在溶液中形成亚硫酸根离子。硫氧化物是其他污染物(如柴油废气和细颗粒物)的重要成分。

目的

研究亚硫酸盐对培养的肥大细胞(大鼠嗜碱性白血病[RBL-2H3]细胞)和人外周血嗜碱性粒细胞的细胞反应。

方法

在存在和不存在抗氧化剂及氧化还原代谢抑制剂的情况下,评估亚硫酸盐诱导的肥大细胞脱颗粒和细胞内活性氧的产生。使用β-己糖胺酶、5-羟色胺和组胺释放试验测定脱颗粒情况。使用氧化还原敏感染料2',7'-二氯荧光素二乙酸酯测定细胞内活性氧生成的诱导情况。

结果

亚硫酸钠诱导RBL-2H3细胞脱颗粒并产生细胞内活性氧。这些反应被自由基清除剂四甲基硫脲和黄素酶抑制剂二苯基碘鎓抑制,但不受细胞外钙耗竭的影响。外周血嗜碱性粒细胞在暴露于亚硫酸钠后也显示出组胺释放。

结论

亚硫酸盐作为二氧化硫的水合离子,通过非IgE依赖途径诱导细胞活化,导致肥大细胞脱颗粒。该反应也不同于IgE介导的脱颗粒,因为它对细胞外钙的流入不敏感。推测的途径似乎依赖于还原型烟酰胺腺嘌呤二核苷酸磷酸氧化酶复合物的激活,导致细胞内氧化应激。

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