FREE RADICALS IN CELLULAR INJURY BY MINERAL PARTICLES

自由基在细胞损伤中的作用 矿物颗粒和金属离子。他们证明了 羟基自由基，由金属介导的类芬顿反应产生， 在硅诱导活化机理中起重要作用 核转录因子NF κ B。之前报告的 肿瘤坏死因子-α（TNF）抑制石英诱导的 BALB/3 T3细胞的肿瘤转化在 TNF诱导锰依赖性超氧化物的基础 歧化酶（Mn-SOD）。石英诱导相变对 其强抑制作用表现为氧自由基机制 被自由基清除剂二甲亚砜所破坏的属性， 结晶二氧化硅表面化学直接决定了其 通过对方石英样品的测试显示了生物活性， 对大鼠肺泡上皮细胞AE 6有较强的毒性， 在800摄氏度加热后失去了大部分活性， 在1300摄氏度加热后完全无毒：热处理 去除了活性表面羟基和取代它们的离子化基团 具有非活性氧桥（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).