Reactive oxygen species: their relation to pneumoconiosis and carcinogenesis

Environ Health Perspect. 1998 Oct;106 Suppl 5(Suppl 5):1151-5. doi: 10.1289/ehp.98106s51151.

Abstract

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.

Publication types

  • Review

MeSH terms

  • Animals
  • DNA Damage
  • Genes, p53
  • Humans
  • Lipid Peroxidation
  • Lung / metabolism
  • Lung Injury
  • Lung Neoplasms / etiology*
  • Lung Neoplasms / genetics
  • Lung Neoplasms / metabolism
  • NF-kappa B / metabolism
  • Pneumoconiosis / etiology*
  • Pneumoconiosis / metabolism
  • Reactive Oxygen Species / metabolism*
  • Transcription Factor AP-1 / metabolism

Substances

  • NF-kappa B
  • Reactive Oxygen Species
  • Transcription Factor AP-1