Sequential changes of lamellar body hydrolases during ozone-induced alveolar injury and repair
Journal Article
·
· Am. J. Pathol.; (United States)
OSTI ID:6071933
Lamellar body hydrolases in acutely damaged and regenerating type II cells were determined using an established rat model with well-defined stages of bronchiolo-alveolar injury and repair. Lamellar bodies were isolated from control and ozone-exposed (3.0 ppm for 8 hours) adult male rats by sucrose density gradient centrifugation and analyzed for their content of six different lysosomal hydrolases. Immediately after 3 ppm ozone exposure (zero-time) there was a significant decrease in specific enzyme activity (units/mg protein) of five lamellar body hydrolases and these activities remained depressed for at least 24 hours after exposure. In addition, total enzyme activity (units/lung) was reduced at zero-time for beta-hexosaminidase and at 24 hours postexposure for alpha-mannosidase and alpha-L-fucosidase. During the reparative and recovery stages (48 to 96 hours) the hydrolases demonstrated variable elevations in both specific activity and total activity (units/lung). Characteristically, beta-hexosaminidase and beta-galactosidase reached supranormal values at 96 hours, whereas alpha-mannosidase remained below normal levels through the recovery stage. Moreover, at 24 to 48 hours the lamellar body fraction demonstrated prominent enzyme depletion relative to the expanding pool of stored surfactant. It is concluded that acute ozone stress initiates the development of hydrolase deficiency within the lamellar bodies of injured and regenerating type II cells. This deficiency state is followed by asynchronous lamellar body hydrolase elevations that reflect distinct patterns of response rather than uniform return to normal condition. The lysosomal enzyme changes of lamellar bodies may be pathogenetically linked to the development of associated alterations in the storage and secretion of surfactant.
- Research Organization:
- Univ. of Pittsburgh, PA (USA)
- OSTI ID:
- 6071933
- Journal Information:
- Am. J. Pathol.; (United States), Journal Name: Am. J. Pathol.; (United States) Vol. 134:5; ISSN AJPAA
- Country of Publication:
- United States
- Language:
- English
Similar Records
Ozone-induced lamellar body responses in a rat model for alveolar injury and repair
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Cerebrohepatorenal Syndrome (CHRS) of Zellweger: lysosomal enzyme activities, sulfation of glycosaminoglycans, and pipecolic acid levels in cultured skin fibroblasts
Journal Article
·
Mon Aug 01 00:00:00 EDT 1988
· Am. J. Pathol.; (United States)
·
OSTI ID:6834851
Ozone-induced alterations of lamellar body lipid and protein during alveolar injury and repair
Journal Article
·
Fri Sep 01 00:00:00 EDT 1989
· Lipids; (USA)
·
OSTI ID:5079358
Cerebrohepatorenal Syndrome (CHRS) of Zellweger: lysosomal enzyme activities, sulfation of glycosaminoglycans, and pipecolic acid levels in cultured skin fibroblasts
Thesis/Dissertation
·
Mon Dec 31 23:00:00 EST 1984
·
OSTI ID:5941210
Related Subjects
560300* -- Chemicals Metabolism & Toxicology
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
ANIMALS
BIOLOGICAL MODELS
BIOLOGICAL STRESS
CELL CONSTITUENTS
CENTRIFUGATION
ENZYME ACTIVITY
ENZYMES
HYDROLASES
MAMMALS
ORGANIC COMPOUNDS
ORGANOIDS
OZONE
PROTEINS
RATS
RODENTS
SEPARATION PROCESSES
TOXICITY
ULTRACENTRIFUGATION
VERTEBRATES
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
ANIMALS
BIOLOGICAL MODELS
BIOLOGICAL STRESS
CELL CONSTITUENTS
CENTRIFUGATION
ENZYME ACTIVITY
ENZYMES
HYDROLASES
MAMMALS
ORGANIC COMPOUNDS
ORGANOIDS
OZONE
PROTEINS
RATS
RODENTS
SEPARATION PROCESSES
TOXICITY
ULTRACENTRIFUGATION
VERTEBRATES