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Alveolar type II cells: effect of silica.

Authors
Rabovsky-J; Ma-JY
Source
NIOSH 1988 Sep; :1-40
Link
NIOSHTIC No.
00186101
Abstract
The role of silica (14808607) in pulmonary disorders at the cellular level was investigated in rat lung. The effect of exposure to silica inhalation on two cytochrome-P450 dependent enzymes (ethoxycoumarin-deethylase and ethoxyphenoxazone-deethylase) in the lung microsomal fraction was studied in male Sprague-Dawley-rats. Exposure to silica had no statistically significant effect on the induction ratio for either activity. Silica exposure may have caused a diminished level of the constitutive enzyme activity in rat lung tissue. Cytochrome-P450 dependent enzymes in the isolated microsomal fraction from whole lung tissue and in isolated rat lung alveolar type-II cells were also studied. Lung microsomal benzyloxyphenoxazone-deethylase was shown to be a nonpolyaromatic hydrocarbon inducible, metyrapone sensitive activity whereas ethoxyphenoxazone-deethylase was a polycyclic aromatic hydrocarbon inducible, alpha-naphthoflavone sensitive form. The alveolar type- II cytochrome-P450 dependent system was tested for its sensitivity to a known purified macrophage secreted compound, platelet activating factor (PAF). PAF exposure enhanced ethoxyphenoxazone- deethylase activity in whole cells but not in microsomal or sonicated whole cell preparations. The effect of PAF may be mediated through a permeability mechanism or through the reversal of an inhibitory process. The authors conclude that a mediator secreted by activated macrophages can affect a critical detoxication mechanism in another cell type of the alveolar region.
Keywords
NIOSH-Author; Lung-cells; Cell-function; Cell-damage; Silica-dusts; Inhalation-studies; Laboratory-animals; Pulmonary-function
CAS No.
14808-60-7
Publication Date
19880901
Fiscal Year
1988
NTIS Accession No.
PB89-188148
NTIS Price
A04
NIOSH Division
DRDS
Source Name
Final Report, Division of Respiratory Disease Studies, NIOSH, 40 pages, 56 references
State
WV
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