Effect of bovine serum albumin on the synthesis of prostaglandin and incorporation of (/sup 3/H)acetate into platelet-activating factor

Journal Article · Tue Sep 01 00:00:00 EDT 1987 · Arch. Biochem. Biophys.; (United States)

DOI:https://doi.org/10.1016/0003-9861(87)90564-9· OSTI ID:5842152

Heinsohn, C; Polgar, P; Fishman, J; Taylor, L

The binding of fatty acids by bovine serum albumin (BSA) is well documented. However, the interaction between the synthesis of prostaglandins (PGs) and the trapping of arachidonate released from cellular lipid stores is not as well understood. In this communication, we relate the trapping of fatty acids to the synthesis of PGs and the incorporation of (/sup 3/H)acetate into platelet-activating factor (PAF). Our results show that, as determined by radioimmunoassay, BSA inhibits bradykinin (BK) (5 ng/ml) and ionophore A23187 (10 microM)-stimulated synthesis of PGs in human embryo lung fibroblasts (IMR-90) in a concentration-dependent manner. Experiments using prelabel with (/sup 3/H)arachidonate followed by extraction and thin-layer chromatography show that, in the presence of 2 mg/ml BSA, IMR-90 release essentially only fatty acid following stimulation with bradykinin. Little if any prostaglandin and no endoperoxide are detected. In the same experiment, in absence of BSA, about 70% of the released label is detected as prostaglandin. alpha-Cyclodextrin, another trapper of fatty acid, inhibits PG synthesis in much the same way. BSA and alpha-cyclodextrin also inhibit prostacyclin synthesis in endothelial cells derived from the calf pulmonary artery. However, the inhibition of PG synthesis in these cells is not as complete as that in the IMR-90. In contrast to the effect of the trappers on PG synthesis, BSA and alpha-cyclodextrin are observed to potentiate BK- and ionophore-stimulated incorporation of (3H)acetate into PAF in the endothelial cells. The labeled PAF is not released from the cells in either the presence or absence of the trappers, leading us to conclude that BSA causes an increase in acetate-labeled cellular PAF by trapping released fatty acid.

• Research Organization: Boston Univ. School of Medicine, MA
• OSTI ID: 5842152
• Journal Information: Arch. Biochem. Biophys.; (United States), Journal Name: Arch. Biochem. Biophys.; (United States) Vol. 257:2; ISSN ABBIA
• Country of Publication: United States
• Language: English

Related Subjects

550201* -- Biochemistry-- Tracer Techniques
59 BASIC BIOLOGICAL SCIENCES
ACETATES
ALBUMINS
ANIMAL CELLS
ANIMALS
ARACHIDONIC ACID
BIOCHEMICAL REACTION KINETICS
BIOLOGICAL FUNCTIONS
BIOSYNTHESIS
BLOOD COAGULATION FACTORS
BODY
BRADYKININ
CARBOXYLIC ACID SALTS
CARBOXYLIC ACIDS
CATTLE
CHROMATOGRAPHY
COAGULANTS
CONNECTIVE TISSUE CELLS
DOMESTIC ANIMALS
DOSE-RESPONSE RELATIONSHIPS
DRUGS
EMBRYOS
FIBROBLASTS
FUNCTIONS
HEMATOLOGIC AGENTS
IMMUNOASSAY
IMMUNOLOGY
ISOTOPE APPLICATIONS
KINETICS
KININS
LABELLED COMPOUNDS
LUNGS
MAMMALS
MAN
MONOCARBOXYLIC ACIDS
ORGANIC ACIDS
ORGANIC COMPOUNDS
ORGANS
PEPTIDES
POLYPEPTIDES
PRIMATES
PROSTAGLANDINS
PROTEINS
RADIOASSAY
RADIOIMMUNOASSAY
RADIOIMMUNOLOGY
REACTION KINETICS
RESPIRATORY SYSTEM
RUMINANTS
SEPARATION PROCESSES
SOMATIC CELLS
SYNTHESIS
THIN-LAYER CHROMATOGRAPHY
TRACER TECHNIQUES
TRITIUM COMPOUNDS
VERTEBRATES