FREE RADICALS IN CELLULAR INJURY BY MINERAL PARTICLES

自由基在大鼠急性脑损伤中作用的研究 包括矿物颗粒和金属离子。他们证明了 由金属介导的类Fenton反应产生的羟基自由基， 在二氧化硅诱导的细胞活化机制中起重要作用 核转录因子NFkB。之前报道的 肿瘤坏死因子-α对石英诱导的抑制作用 对BALB/3T3细胞恶性转化的再评价 肿瘤坏死因子诱导锰依赖超氧化物歧化的基础 超氧化物歧化酶(Mn-SOD)。石英诱导相变的依赖关系 通过对氧自由基的强烈抑制，证实了氧自由基的作用机制。 由自由基清除剂二甲基亚砜。它的属性是 晶态二氧化硅的表面化学直接决定了其表面性质。 方石英样品的测试显示了生物活性， 对大鼠肺泡上皮细胞AE6有较强的毒性，但 在800摄氏度加热后失去了大部分活性， 1300℃加热后完全无毒：热处理 去除活性表面羟基和取代它们的电离基团 带有非活性氧桥(硅氧烷)。

Studies on the role of free radicals in cellular injury caused by mineral particles and metal ions were concluded. They showed that hydroxyl radicals, generated by metal-mediated Fenton-like reactions, play an important role in the mechanism of silica-induced activation of the nuclear transcription factor NFkB. The previously reported inhibition by tumor necrosis factor-alpha (TNF) of quartz-induced neoplastic transformation of BALB/3T3 cells was re-evaluated on the basis of the induction by TNF of manganese-dependent superoxide dismutase (Mn-SOD). The dependence of quartz-induced transformation on an oxygen radical mechanism was demonstrated by its strong inhibition by the free radical scavenger, dimethylsulfoxide. That properties of the surface chemistry of crystalline silica directly determine its biological activity was shown by tests on a sample of cristobalite, which was highly toxic on rat lung alveolar epithelial AE6 cells, but lost most of its activity after heating at 800 degrees C and was completely nontoxic after heating at 1300 degrees C: the heat treatment removed the reactive surface hydroxyl and ionized groups replacing them with unreactive oxygen bridges (siloxanes).