Vallyathan V, Shi X, Castranova V
Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505, USA.
Environ Health Perspect. 1998 Oct;106 Suppl 5(Suppl 5):1151-5. doi: 10.1289/ehp.98106s51151.
Occupational exposures to mineral particles cause pneumoconiosis and other diseases, including cancer. Recent studies have suggested that reactive oxygen species (ROS) may play a key role in the mechanisms of disease initiation and progression following exposure to these particles. ROS-induced primary stimuli result in the increased secretion of proinflammatory cytokines and other mediators, promoting events that appear to be important in the progression of cell injury and pulmonary disease. We have provided evidence supporting the hypothesis that inhalation of insoluble particles such as asbestos, agricultural dusts, coal, crystalline silica, and inorganic dust can be involved in facilitating multiple pathways for persistent generation of ROS, which may lead to a continuum of inflammation leading to progression of disease. This article briefly summarizes some of the recent findings from our laboratories with emphasis on the molecular events by which ROS are involved in promoting pneumoconiosis and carcinogenesis.
职业接触矿物颗粒会导致尘肺病和其他疾病，包括癌症。最近的研究表明，活性氧（ROS）可能在接触这些颗粒后疾病的起始和进展机制中起关键作用。ROS诱导的主要刺激导致促炎细胞因子和其他介质的分泌增加，促进了在细胞损伤和肺部疾病进展中似乎很重要的事件。我们提供了证据支持这样的假设，即吸入不溶性颗粒，如石棉、农业粉尘、煤、结晶硅石和无机粉尘，可能参与促进ROS持续产生的多种途径，这可能导致炎症的持续发展，进而导致疾病进展。本文简要总结了我们实验室最近的一些发现，重点是ROS参与促进尘肺病和致癌作用的分子事件。
