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Chronic exposure to mineral particles may cause development of pulmonary inflammation both in humans and experimental animals. Inhalation of mineral particles results in their uptake by alveolar macrophages. Moreover, a small part of the particles may be taken up also be the epithelial cells lining the pulmonary alveoli (see Doelman et al., 1990). The phagocytized mineral particles may induce inflammatory reaction during which chemotactic factors are released from the macrophages. Upon stimulation by macrophage-derived cytokines leukocytes infiltrate to the site of inflammation in the lung (Lugano et al., 1982). Prolonged exposure to mineral particles is associated with accumulation of activated phagocytic cells, i.e. neutrophils, eosinophils and basophils, in the lungs. Activation of alveolar macrophages by mineral fibers may be of particular importance in the pulmonary inflammation and fibrosis because they are the first line of defence against foreign intruders (Doelman et al., 1990). Furthermore, activation of macrophages and other phagocytic cells, monocytes and polymorphonuclear leukocytes (PMNL), results in a release of proteolytic enzymes and reactive oxygen metabolites (ROM) such as superoxide anion radical, hydrogen peroxide, hydroxyl radical and singlet oxygen (Adamson and Bowden, 1988) which contribute to oxidative stress in phagocytes (Halliwell and Gutteridge, 1984; Seifert and Schultz, 1991). |
