title: The effect of stone-wool on rat lungs and on the primary culture of rat alveolar macrophages and type II pneumocytes.
abstract: The effect of stone-wool has been studied in both in vivo long term sequential and in vitro methods in male Sprague-Dawley rats. Stone-wool was administered by single intratracheal instillation and the lungs were examined after 1, 3 and 6 months of exposure by morphological methods. UICC crocidolite was applied as a positive control. In addition, the effects of both fibres were examined in primary cultures of alveolar macrophages (AM) and type II pneumocytes (T2) by morphological, biochemical and immunological methods. By the end of 6 months stone-wool induced moderate pulmonary interstitial inflammation and fibrosis without progression, whereas crocidolite induced progressive interstitial inflammation and fibrosis as a function of time. Although stone-wool inhibited phagocytosis, it did not induce serious membrane damage to the cells examined and did not destroy their ultrastructure. It significantly reduced the activity of Cu,Zn/superoxide dismutase (SOD) and alkaline phosphatase (AP) in alveolar macrophages and significantly decreased the activity of AP and gamma-glutamyl transpeptidase (GGT) in type II pneumocytes. Crocidolite, on the other hand, decreased the activity of all enzymes (glutathione peroxidase, GSH-Px; glutathione reductase, GSH-Rd) of glutathione metabolism as well as alkaline phosphatase in alveolar macrophages. It decreased the activity of all enzymes in type II pneumocytes, except for Cu,Zn/SOD. On exposure to stone-wool, the production of inflammatory proteins, macrophage chemoattractant protein-1 (MCP-1) and macrophage inhibitory protein-1alpha (MIP-1alpha) increased in both cultured cells but did not reach the level induced by crocidolite. Our results suggested that stone-wool is less toxic than crocidolite. Whether it is carcinogenic or not, is still an open question.
authors.affiliation: Fodor József National Center for Public Health, Budapest, Hungary. tatrai@fjokk.hu
authors.forename: Erzsébet
authors.initials: E
authors.lastname: Tátrai
authors.forename: Márta
authors.initials: M
authors.lastname: Brozik
authors.forename: Agnes
authors.initials: A
authors.lastname: Drahos
authors.forename: Zuzana
authors.initials: Z
authors.lastname: Kováciková
authors.forename: Eva
authors.initials: E
authors.lastname: Six
authors.forename: Márta
authors.initials: M
authors.lastname: Csík
authors.forename: Annamária
authors.initials: A
authors.lastname: Dám
mesh_terms: D000818:Animals; D002462:Cell Membrane / Q000187:drug effects / Q000473:pathology; D018932:Chemokine CCL2 / Q000378:metabolism; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D008168:Lung / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology / Q000648:ultrastructure; D008198:Lymph Nodes / Q000187:drug effects / Q000648:ultrastructure; D019402:Macrophage Inflammatory Proteins / Q000378:metabolism; D016676:Macrophages, Alveolar / Q000187:drug effects* / Q000201:enzymology / Q000648:ultrastructure; D008297:Male; D008855:Microscopy, Electron, Scanning; D046529:Microscopy, Electron, Transmission; D019016:Mineral Fibers / Q000633:toxicity*; D011658:Pulmonary Fibrosis / Q000139:chemically induced* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D019402:Macrophage Inflammatory Proteins; D019016:Mineral Fibers