Abstract
Oral administration of methacrylonitrile (MeAN) (100mg/kg body wt/day) to rats for 14 days damaged the lung tissue and altered the bronchoalveolar lavage (BAL) angiotensin-converting enzyme activity (ACE) and levels of phospholipids and surfactant phospholipids. However, there was no alteration in BAL lactate content or lactate dehydrogenase activity. A significant increase in the phosphatidylcholine content in the extracellular surfactant indicates Type-II cell proliferation. MeAN caused the lung injury by increasing alveolar capillary permeability and promoting the accumulation of surfactant phospholipids, which may lead to serious conditions such as fibrosis.
