[The role of macrophages in asbestos-induced carcinogenesis].
Data available on the pathways of asbestos (fibrous) carcinogenesis still leaves much to be desired. Asbestos is regarded as a non-genotoxic substance by most researchers. There is insufficient evidence on the interaction of fibres, target-cells and macrophages. Macrophages secreted proteins (ca. 450 kD) to inhibit proliferation of intact mesothelium and cytoxine (3-5 kD) which stimulated the cellular sensitivity of intact mesothelium and mesotheliomas to the toxic influence of asbestos. It was suggested that the effect was due to the triggering of intrinsic causation of cell death. Like any other fibres, carcinogenic effect of asbestos could be accounted for by such significant factor as active oxygen radicals. When exposed to asbestos, both intact mesothelial and mesothelioma cells and macrophages synthesized those substances. Free radical-like substances in conjunction with macrophage-conditioned media produced toxic effect on mesothelial cells. The role of active oxygen radicals in fibre-induced carcinogenesis is discussed.
Pylev
L N
LN
Vasil'eva
L A
LA
Stadnikova
N M
NM
Smirnova
O V
OV
D000818:Animals; D001194:Asbestos / Q000009:adverse effects*; D002273:Carcinogens / Q000009:adverse effects*; D002471:Cell Transformation, Neoplastic; D002478:Cells, Cultured; D004848:Epithelium / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D005260:Female; D017737:Macrophages, Peritoneal / Q000378:metabolism*; D008654:Mesothelioma / Q000139:chemically induced* / Q000378:metabolism*; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D014407:Tumor Cells, Cultured
D002273:Carcinogens; D017382:Reactive Oxygen Species; D001194:Asbestos