Hyperoxia alters effect of calcium on rat alveolar macrophage superoxide production.
Hyperoxia alters effect of calcium on rat alveolar macrophage superoxide production.
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高氧改变钙对大鼠肺泡巨噬细胞超氧化物产生的影响。
DOI：
10.1152/jappl.1986.60.4.1300
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Harrison,G
中科院分区：
文献类型：
--
作者：
Forman,HJ;Nelson,J;Harrison,G
研究了高氧对超氧阴离子自由基（O2-.）研究了大鼠肺泡巨噬细胞的产生（呼吸爆发）。细胞外Ca ~（2+）对刀豆蛋白A（conA）刺激的呼吸爆发的增强作用被O_2暴露抑制。同样，维拉帕米对con A刺激的呼吸爆发的抑制作用也因O2暴露而降低。O2暴露也抑制conA刺激，这是独立的Ca 2+的进入。暴露于O2也导致O2-下降。由A23187或佛波醇肉豆蔻酸酯乙酸酯（PMA）刺激产生。随着A23187刺激，细胞外Ca 2+是必不可少的空气暴露（对照）或O2暴露的细胞。PMA的刺激是独立的细胞外Ca 2+的空气或O2暴露的巨噬细胞和维拉帕米没有抑制。测定对照组和O2暴露组肺泡巨噬细胞内游离钙浓度（[Ca 2 +]i）。高氧暴露没有改变[Ca 2 +]i在未刺激的细胞。在对照组中，Con A刺激[Ca 2 +]i立即增加，随后迅速下降，第二次上升和下降。维拉帕米、乙二醇-双（β-氨乙基醚）-N，N′-四乙酸或O2暴露可抑制第二次升高。呼吸爆发试验和测量的conA刺激的变化[Ca 2 +]i的结果表明，参与刺激-反应耦合的Ca 2+进入细胞O2毒性抑制。
The effect of hyperoxia on the Ca2+ dependence of stimulated superoxide anion radical (O2-.) production (the respiratory burst) of rat alveolar macrophages was investigated. Enhancement of the concanavalin A (con A)-stimulated respiratory burst by extracellular Ca2+ was suppressed by O2 exposure. Similarly, the inhibitory effect of verapamil on the con A-stimulated respiratory burst was reduced by O2 exposure. O2 exposure also inhibited con A stimulation that was independent of Ca2+ entry. Exposure to O2 also caused a decline in O2-. production stimulated by either A23187 or phorbol myristate acetate (PMA). With A23187 stimulation, extracellular Ca2+ was essential for either air-exposed (control) or O2-exposed cells. With PMA, stimulation was independent of extracellular Ca2+ for either air or O2-exposed macrophages and verapamil did not inhibit. Free intracellular Ca2+ concentration ([Ca2+]i) was measured in control and O2-exposed alveolar macrophages. Hyperoxic exposure did not alter [Ca2+]i in unstimulated cells. In controls, con A stimulated an immediate increase in [Ca2+]i followed by a rapid decrease and a second rise and fall. The second elevation was suppressed by verapamil or ethyleneglycol-bis (beta-aminoethylether)-N,N′-tetraacetic acid or O2 exposure. The results of both the respiratory burst assays and measurement of con A-stimulated changes in [Ca2+]i suggest that Ca2+ entry involved in stimulus-response coupling is suppressed in cellular O2 toxicity.