-transparent.png){kind=logo}
The turnover of phospholipid fatty acid moieties of bone marrow-derived macrophages was analyzed by separate determination of degrading and acylating activities. Acylating activities were followed in intact cells by incubation with excess arachidonic acid and degradation of phospholipids was followed in cells prelabeled with fatty acids. Significant phospholipase A2 activity was detectable only if the reutilization of liberated fatty acid was inhibited , e.g. by p-chloromercuribenzoate. It was of interest that the divalent cation ionophore A 23187 and various antiphlogistic drugs like indomethacin, diclofenac, and acetylsalicylic acid were found to inhibit the acylation reaction. These compounds led to increased levels of free arachidonic acid in stimulated, as well as in unstimulated cells. Increased activities of phospholipase A2 were achieved by treatment with the bivalent cation ionophore A 23187 and with zymosan. The effect of zymosan obtained from various sources was found to be exclusively due to contamination of tee zymosan particles with phospholipase A2 activity. Even when the cellular phospholipase activity was increased by the addition of exogenous phospholipase activity contained in the zymosan particles, degradation of cellular phospholipids was not measurable unless the reacylation was inhibited. These results suggest that in the cells studied, the level of free arachidonic acid is mainly controlled by the activity of the lysophosphatide acyltransferase.
E E Kröner, and
B A Peskar, and
H Fischer, and
E Ferber
April 1990,
Biological chemistry Hoppe-Seyler,
E E Kröner, and
B A Peskar, and
H Fischer, and
E Ferber
December 2009,
Biochimica et biophysica acta,
E E Kröner, and
B A Peskar, and
H Fischer, and
E Ferber
October 1994,
Bioscience, biotechnology, and biochemistry,
E E Kröner, and
B A Peskar, and
H Fischer, and
E Ferber
January 1997,
Methods in molecular biology (Clifton, N.J.),
E E Kröner, and
B A Peskar, and
H Fischer, and
E Ferber
January 1990,
Methods in molecular biology (Clifton, N.J.),
E E Kröner, and
B A Peskar, and
H Fischer, and
E Ferber
January 1983,
Advances in prostaglandin, thromboxane, and leukotriene research,
E E Kröner, and
B A Peskar, and
H Fischer, and
E Ferber
January 1989,
Advances in experimental medicine and biology,
E E Kröner, and
B A Peskar, and
H Fischer, and
E Ferber
October 1985,
Biochimica et biophysica acta,
E E Kröner, and
B A Peskar, and
H Fischer, and
E Ferber
January 1981,
Cellular immunology,
E E Kröner, and
B A Peskar, and
H Fischer, and
E Ferber
August 2011,
Particle and fibre toxicology,
