Collagen metabolism in rat lungs during chronic intermittent exposure to oxygen.
Collagen metabolism was studied in rat lungs during prolonged intermittent exposure to oxygen. After an initial of 2-d exposure to oxygen, the rats alternately breathed air and oxygen in 24-h periods up to 30 d. Lung histology showed perivascular edema as an early sign of oxygen toxicity. Increased capillary permeability was followed by a marked perivascular leukocytosis that was prominent between the 5th and 11th d of the treatment. During the further course of the experiment, the inflammatory response gradually diminished, and finally a network of collagen fibres filled the perivascular areas. The inflammatory process elevated the amounts of DNA and RNA in lung tissue, and the ratio of RNA to DNA was maximal on the 5th day. Studies on metabolism of lung collagen with intraperitoneally injected 3H-proline as label showed that, after the initial inflammatory reaction, both synthesis and degration of collagen were increased in oxygen-treated lungs. The increase in synthesis exceeded the rise in degradation and, therefore, collagen was accumulated. The activation of lung collagen synthesis coincided in time with a rise in the activity of lung protocollagen proline hydroxylase.
D000818:Animals; D003094:Collagen / Q000378:metabolism*; D004247:DNA / Q000378:metabolism; D006909:Hydroxyproline / Q000378:metabolism; D008168:Lung / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D009584:Nitrogen / Q000378:metabolism; D010100:Oxygen / Q000633:toxicity; D011393:Procollagen-Proline Dioxygenase / Q000378:metabolism; D011392:Proline / Q000378:metabolism; D011654:Pulmonary Edema / Q000139:chemically induced; D012313:RNA / Q000378:metabolism; D051381:Rats; D014316:Tritium
D014316:Tritium; D012313:RNA; D003094:Collagen; D004247:DNA; D011392:Proline; D011393:Procollagen-Proline Dioxygenase; D009584:Nitrogen; D006909:Hydroxyproline; D010100:Oxygen