Alveolar type II cells: effects of silica. Type II cell phospholipid metabolism: possible involvement in silica-induced phospholipidosis.
Final Report 1988 Sep; :1-28
The effects of the drug tetrandrine on the phospholipid content of the extracellular surfactant of silica (14808607) exposed rats was studied to elucidate the mechanisms of silicosis and the protective effect offered by tetrandrine. Male Sprague-Dawley-rats were injected intratracheally with silica at 50mg/kg and sacrificed 1 month later. Others were pretreated with 7.5 milligrams/rat/day of tetrandrine injected orally for 5 days and allowed to recover 1 day before silica exposure. Drug treated rats were exposed either to air or to silica inhalation at about 80mg/m3 for 6 hours. The results indicated that phospholipidosis may be attributed to the impairment of normal phospholipid degradation in the lung, and that such impairment is resulted from the binding of the lipids to small amphiphilic molecules. The binding phenomenon altered the surface active properties of the phospholipids and was of biochemical significance. The fact that in silica treated animals, phospholipidosis occurred at times long after the dose but not at the onset further suggested the intricate process involving the lung surfactant. According to the author, silica dust may cause sustained release of amphiphilic molecules from cells and tissues. These molecules in turn bind to phospholipids and prevent them from undergoing normal degradation.
NIOSH-Contract; Pulmonary-system-disorders; Lung-disorders; Mineral-dusts; Laboratory-animals; Inhalation-studies; Silica-dusts; Dust-inhalation; Phospholipids; Lipid-disorders
NTIS Accession No.
Asthma and Chronic Obstructive Pulmonary Disease; Disease and Injury; Pulmonary-system-disorders;
Final Report, 28 pages, 32 references