摘要
超细颗粒已被证明在体内和体外诱导前炎症效应。促炎基因表达的增加可能需要特定转录因子的激活,如核因子kappaB (NF-kappaB),通过一些可能的途径,包括Ca2+和活性氧物种。用荧光染料呋喃2测定人单核细胞Monomac 6细胞系暴露于66微克x毫升(-1)的超细炭黑(ufCB;直径14nm)、炭黑(CB;直径260纳米),石英(直径1.45微米),或介质单独。UfCB而非fine CB诱导Monomac 6细胞内静息Ca2+浓度增加1.6倍(p<0.01)。此外,ufCB诱导内质网Ca2+-腺苷三磷酸酶(ATPase)抑制剂thapsigargin的响应增加2.6倍(p<0.001),表明Ca2+释放激活的Ca2+电流通过质膜增强。这种反应被细胞外Ca2+的去除和Ca2+通道阻断剂维拉帕米所抑制。此外,ufCB刺激细胞外Mn2+的进入。最后,抗氧化剂甘露醇和nacystelin均能抑制ufCB对thapsigargin的反应。 These data suggest that ultrafine carbon black particles stimulated an increase in cytosolic Ca2+, possibly through the entry of extracellular Ca2+ via Ca2+ channels in the plasma membrane. The particles may in part activate the opening of Ca2+ channels via a mechanism involving reactive oxygen species.