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Title	Phospholipid interactions in lamellated osmiophilic inclusion bodies from fetal lung type II alveolar epithelium and their clinical implication
Author	Fleming, James Kenneth
Date	1988
Affiliation/College	College of Graduate Studies
Department	Molecular and Cellular Biology and Pathobiology
Extent	166 leaves : ill. plates; 29 cm
Source	QU 93 F597p 1988
Subject.MeSH	Phospholipids Fetal Organ Maturity Academic Dissertations
Collection	MUSC Theses and Dissertations
Contributing Institution	Waring Historical Library (MUSC)
Rights	Copyright is held by the author.
Language	English
Type	Text
Format	application/pdf
Media Type	Manuscripts
Resource Identifier	mtd1988_fleming_jk
Abstract	The methodology for the measurement of the specific phospholipids: total choline phospholipid, phosphatidylcholine, sphingomyelin and phosphatidylglycerol has been advanced to permit micromolar quantitation. Phospholipids mass is measured by enzymatic hydrolysis resulting in the generation of hydrogen peroxide and subsequent reduction by a peroxidase indicator reaction. Uric acid represents a major interferent to the indicator sequence: H202 + p-hydroxyphenylacetic acid ___peroxidase___> fluorescence only when micromolar concentrations of peroxide are generated. The mechanism has been shown to involve the reduction of hydrogen peroxide. The application of these methods has solved several biochemical dilemma in understanding the phospholipid metabolism in the maturing fetal lung. The difference between the measurement of phospholipid in amniotic fluid and the same measurement performed on isolated lamellar bodies represents the distinction between phospholipid of extra-pulmonary origin and that of pulmonary origin. This difference plays a vital role in the assessment of the fetal lung maturity. The difference is greater in those infants born with immature lungs and in those infants born to noncompliant insulin dependent diabetic mothers. As the lung matures, increasing synthesis of pulmonary phospholipid from type II alveolar cells causes the magnitude of this difference to decline. Apolipoprotein-AI and to a lesser extent apolipoprotein-AII from maternal serum were also detected in human amniotic fluid, which along with their accompanying lipids, increase slightly with gestational age. Their presence is eventually overshadowed in concentration as pulmonary surfactant is secreted by the maturing fetal lung. Using fetal and newborn rat lung models, it was found that insulin activates phospholipase A2, thereby diminishing the absolute concentration of phosphatidylcholine and diminishing the phosphatidylcholine/lysophosphatidylcholine ratio. Phosphatidylcholine declines, because it is functioning as a primary substrate in its conversion to lysophosphatidylcholine. This fact has further implications on the fluidity of the lamellar membranes. The viscosity of lamellar structures is altered by changes in the phosphatidylcholine/lysophosphatidylcholine ratio. Higher viscosities occur when the phosphatidylcholine/lysophosphatidylcholine ratio was reduced, as occur in non-controlled diabetics who have frequent episodes of hyperinsulinemia. The higher viscosity could hinder unravelling of the secreted lamellar membranes and contribute to the development of respiratory distress syndrome.

Phospholipid interactions in lamellated osmiophilic inclusion bodies from fetal lung type II alveolar epithelium and their clinical implication

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