Changes in phospholipid biosynthetic enzyme activity in lung tissue and isolated lung cells of rats after exposure to nitrogen dioxide

Technical Report · Thu Jan 01 04:00:00 EST 1981

OSTI ID:6863398

Wright, E S

The effect of acute exposure to NO/sub 2/ on PL biosynthesis was examined by measuring activities of enzymes of the phosphatidylcholine (PC) and phosphatidylglycerol (PG) biosynthetic pathways in rat lung and liver tissue and in isolated lung cells. Two days after exposure to 42 ppM NO/sub 2/, DNA content of NO/sub 2/-exposed lungs increased 33% while protein in lung homogenate and subcellular fractions was about double control values. Total lung activities of all enzymes measured were 80 to 180% higher in NO/sub 2/-exposed lungs, with the greatest increase occurring in the activity of glycerol-3-phosphate acyltransferase. No changes in any of the measured parameters were observed in liver due to NO/sub 2/ exposure. The activities of biosynthetic and subcellular marker enzymes measured in homogenates and subcellular fractions were depressed immediately at the end of a 5 hr exposure to 40 ppM NO/sub 2/ and 6, 12 and 24 hours later, suggesting direct toxicity of NO/sub 2/ to phospholipid biosynthetic system. Comparison of enzyme activities in isolated Type II cells, macrophages and whole lung homogenate suggests that in rat lung, enzymes of PC synthesis are distributed more or less evenly in different lung cell types, while PG synthesis is localized in Type II cells and may be regarded as an enzymatic marker for that cell type. A general increase in PL biosynthetic enzyme activities was observed in Type II cells isolated from rat lungs 48 hrs after exposure to 40 ppM NO/sub 2/, but not in macrophages. These results are consistent with a specific stimulation of surfactant PL biosynthesis in Type II cells 2 days after NO/sub 2/ exposure, when increased numbers of Type II cells are present in the lung due to proliferation. The general increase in lung content of PL biosynthetic enzymes 48 hrs after NO/sub 2/ exposure was due to both the proliferation of Type II cells and the specific stimulation of biosynthetic enzyme activities within Type II cells. 58 references, 7 figures, 18 tables.

• Research Organization: Rochester Univ., NY (USA). Dept. of Radiation Biology and Biophysics
• DOE Contract Number: AC02-76EV03490
• OSTI ID: 6863398
• Report Number(s): DOE/EV/03490-2067; ON: DE84016266
• Country of Publication: United States
• Language: English

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63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
ACUTE EXPOSURE
ANIMALS
BIOCHEMISTRY
BIOLOGICAL EFFECTS
BIOSYNTHESIS
BODY
CHALCOGENIDES
CHEMISTRY
DATA
ENZYME ACTIVITY
EXPERIMENTAL DATA
INFORMATION
LIPIDS
LUNGS
MAMMALS
MICE
NITROGEN COMPOUNDS
NITROGEN DIOXIDE
NITROGEN OXIDES
NUMERICAL DATA
ORGANIC COMPOUNDS
ORGANS
OXIDES
OXYGEN COMPOUNDS
RESPIRATORY SYSTEM
RODENTS
SYNTHESIS
TIME DEPENDENCE
VERTEBRATES