To one group of CFY male rats bentonite with a high content of aluminium silicate and in another group pure silica dust was given endotracheally. It was established that histological changes that develop within 12-72 hours as a consequence of the effect of non-silicogenic bentonite and silicogenic silica were similar. Lipid and phospholipid content of the lung tissue showed a mild increase in both groups. The characteristic inflammatory reaction in the first 14-24 hours consisted mainly of leukocytes; macrophages appeared later, within 48-72 hours. Dust particles were phagocytized both by leukocytes and macrophages. After 72 hours confluent bronchopneumonia with necrosis developed. 90 days after the bentonite exposure foci of storage, and after the silica exposure, progressive fibrosis of the lung was found. As an effect of silica inhalation the lipid and phospholipid content of the lung tissue increases the ratio of phospholipid fractions changes. Bentonite does not influence the lipid and phospholipid content of the lung tissue. Considering the intense positive aldehyde-bisulfite-toluidine blue reaction of macrophages, it was assumed that the surface of the bentonite particles released from the necrotizing leukocytes have an oriented polysaccharide and/or protein capsule protecting the macrophage from the cytotoxic (necrotizing) effect of bentonite.
|Number of pages||8|
|Journal||Morphologiai es Igazsagugyi Orvosi Szemle|
|Publication status||Published - Jan 1 1983|
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