柴油机排气颗粒对血管内皮细胞病理生理学效应的作用机制。
Mechanism of pathophysiological effects of diesel exhaust particles on endothelial cells.
机构信息
University of Shizuoka, Graduate School of Health Sciences, 52-1 Yada, Shizuoka 422-8526, Japan.
出版信息
Environ Toxicol Pharmacol. 1998 Oct;6(2):117-23. doi: 10.1016/s1382-6689(98)00027-1.
The suspension of diesel exhaust particles (DEP) inhibited endothelium-dependent relaxation (EDR). The mechanism of the impairment of EDR by DEP was investigated with cultured porcine endothelial cells (PEC) and NO synthase (NOS) cell free system. Incubation of PEC with DEP (50-150 μg/ml) for 10-30 min did not induce cell damage. Bradykinin-induced endothelium-dependent relaxing factor (EDRF) release from PEC was bioassayed by cyclic GMP formation in RFL-6 cells. A 10-min preincubation of PEC with DEP (0.1-100 μg/ml) inhibited EDRF release. NOS activity from rat cerebellum cytosol was measured either by the conversion of 3H-l-arginine to (3)H-l-citrulline or the NO(2)(-) formation. A 10-min preincubation of NOS with DEP (0.1-100 μg/ml) did not affect the formation of (3)H-l-citrulline. In contrast, it inhibited NO(2)(-) formation. These results suggest that DEP neither induced cell damage nor inhibited EDRF release from PEC, but DEP scavenged NO to block its physiological action.
柴油废气颗粒（DEP）的悬浮液抑制了内皮依赖性松弛（EDR）。使用培养的猪内皮细胞（PEC）和一氧化氮合酶（NOS）无细胞体系研究了 DEP 损伤 EDR 的机制。PEC 与 DEP（50-150μg/ml）孵育 10-30 分钟不会引起细胞损伤。用 RFL-6 细胞中环磷酸鸟苷形成来生物测定 PEC 中缓激肽诱导的内皮依赖性松弛因子（EDRF）释放。DEP（0.1-100μg/ml）预处理 10 分钟可抑制 EDRF 释放。通过 3H-精氨酸转化为（3）H-瓜氨酸或 NO2（-）形成来测量来自大鼠小脑胞质的 NOS 活性。NOS 与 DEP（0.1-100μg/ml）孵育 10 分钟不会影响（3）H-瓜氨酸的形成。相反，它抑制了 NO2（-）的形成。这些结果表明，DEP 既不诱导细胞损伤，也不抑制 PEC 中 EDRF 的释放，但 DEP 清除了 NO，阻止了其生理作用。
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