马拉硫磷代谢物对人和大鼠嗜碱性细胞脱颗粒和介质释放的影响。

S Xiong, K Rodgers
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引用次数: 21

摘要

本研究检测了马拉硫磷及其衍生物对RBL-1细胞、大鼠腹膜肥大细胞(RPMC)、人外周血嗜碱性粒细胞(hphbb)和皮肤肥大细胞释放组胺和β -己糖氨酸酶的影响。RBL-1细胞与除马拉硫磷和马拉硫磷单酸外的所有有机磷化合物孵育1小时,导致组胺释放增加。β -己糖氨酸酶是一种由嗜碱性细胞释放的酶,也是脱颗粒的生化标记物,在暴露于有机磷化合物1小时后,RBL-1细胞不释放β -己糖氨酸酶。在4小时内,所有测试的化合物都增加了组胺和-己糖氨酸酶的释放。长时间的暴露导致导致介质释放所需的化合物浓度降低。除了马拉硫磷单酸和马拉硫磷(30分钟)或马拉硫磷单酸(1小时)外,RPMC暴露于有机磷化合物会导致组胺的释放,但不会导致-己糖氨酸酶的释放。与马拉硫磷(总组胺释放量51.4 +/- 2.8%)、马拉硫磷二酸(25.7 +/- 2.9%)、-马拉硫磷一酸(31.4 +/- 2.8%)和异马拉硫磷(57.1 +/- 17.1%)孵育1 h,组胺释放量显著增加。孵育1小时后,只有丙拉松和异马拉硫松引起HPBB β -己糖氨酸酶释放。皮肤肥大细胞与丙二醇和β -单酸孵育4小时,导致组胺和β -己糖氨酸酶的释放增加,其水平与化合物48/80相当。这些数据表明,马拉硫磷代谢物可以引起来自各种来源和物种的嗜碱性细胞快速释放组胺。随着孵育时间的延长,马拉硫磷本身引起肥大细胞介质的释放,这表明细胞可能具有代谢马拉硫磷的能力。这些数据还表明,有机磷颗粒对两种不同的肥大细胞介质的释放动力学存在差异,并且介质的释放机制也存在差异。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of malathion metabolites on degranulation of and mediator release by human and rat basophilic cells.

In the present study, the effects of malathion and malathion derivatives on histamine and beta-hexosaminidase release by RBL-1 cells, rat peritoneal mast cells (RPMC), and human peripheral blood basophils (HPBB) and cutaneous mast calls were examined. One hour of incubation of RBL-1 cells with all organophosphate compounds tested, except for malathion and malathion monoacid, led to an increase in histamine release. beta-Hexosaminidase, an enzyme released by basophilic cells and a biochemical marker of degranulation, was not released from RBL-1 cells after 1 h of exposure to organophosphate compounds. Within 4 h, all compounds tested increased the release of histamine and beta-hexosaminidase. Longer exposures led to a decrease in the concentration of the compound that was required to cause mediator release. Exposure of RPMC to organophosphate compounds, with the exception of malathion monoacid and malathion (30 min) or malathion monoacid (1 h), led to the release of histamine, but not beta-hexosaminidase. Incubation of HPBB with malaoxon (51.4 +/- 2.8% total histamine released), malathion diacid (25.7 +/- 2.9%), beta-malathion monoacid (31.4 +/- 2.8%), and isomalathion (57.1 +/- 17.1%) for 1 h led to the release of histamine. Only malaoxon and isomalathion caused beta-hexosaminidase release from HPBB after a 1-h incubation. Incubation of cutaneous mast cells with malaoxon and beta-monoacid for 4 h led to increased release of histamine and beta-hexosaminidase at levels comparable to compound 48/80. These data suggest that malathion metabolites can cause rapid release of histamine from basophilic cells from a variety of origins and species. With prolonged incubation, malathion itself caused the release of mast-cell mediators, suggesting that the cells may be capable of metabolizing malathion. These data also indicate a disparity between the release kinetics of two different mast-cell mediators contained in granules by organophosphates, and that there are different mechanisms of mediator release.

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