New supposition about pathogenesis of pulmonary occupational diseases of dust etiology

Abstract

Initial molecular mechanisms of fibrogenic dust action on organism are based on prolonged formation of reactive oxygen species (RO S) in lungs. This phenomena is based on three processes. The first process is conditioned by activation of phagocytes with dust particles. The action is occurred by means of weak chemical interaction during contacts of the dust particle surface with the cell membrane. The second process is coupled with transformation of formed ROS on catalytic centres of the particle border layer. The third one is copupled with the energy defficit state and intracellular hypoxia development in the koniophage. The mentioned process plays a dominating role in koniophage death. The predominating forms of formed reactive oxygen depends on the chemical content, the molecular structure, and surface properties of dust particles. Generally, coal dust generates the superoxide oxygen anion-radical, quartz one generates hydrogen peroxid (H₂O₂), and asbest one initiates the hydroxilic HO radical. The formed ROS under the fibrogenic dust influence not only causes koniophage death, but stimulates synthesis of interleukine I and other intermediaters regulating the growth of lymphocytes and fibroblasts. The ROS are the cause of relative deficit of proteasa inhibitors and also the cause of appearance of antigens as a result of oxidative protein modification with hydrogen peroxid. All the fibrogenic dusts are characterized by the ROS featured ability of causing the development of more and less manifestated local and generalized mutagen effects. The ROS plays a role indetermination of the ways and methods concerning the respirable dust fraction excretion from lung. They plays a role in localisation of pathologic changes and in manifestations of the diseases developing under the fibrogenic various type dust influence.