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L E HOKIN

Publications and source records attributed to L E HOKIN.

At least 37 records · Page 2Linked to original sources
PubMed1960

Studies on the carrier function of phosphatidic acid in sodium transport. I. The turnover of phosphatidic acid and phosphoinositide in the avian salt gland on stimulation of secretion.

Incubation of slices of the salt gland of the albatross with acetylcholine, which is the physiological secretogogue for this tissue, led to a 13-fold increase in the rate of incorporation of P(32) into phosphatidic acid and a 3-fold increase in the incorporation of P(32) and inositol-2-H(3) into phosphoinositide. The incorporation of P(32) into phosphatidyl choline and phosphatidyl ethanolamine was increased relatively slightly or not at all. Respiration was doubled. The "phospholipid effect" occurred in the microsome fraction, which is known to contain fragments of the endoplasmic reticulum. The enzymes, diglyceride kinase and phosphatidic acid phosphatase, which catalyze the stimulated turnover of phosphatidic acid in brain cortex, were also found in highest concentration in the microsome fraction. The phosphatides which respond to acetylcholine are bound to protein in the membrane. On the basis of these findings it appears that phosphatidic acid and possibly phosphoinositide participate in sodium transport. A scheme, termed the phosphatidic acid cycle, is presented as a working hypothesis, in which the turnover of phosphatidic acid in the membrane, catalyzed by diglyceride kinase and phosphatidic acid phosphatase, functions as a sodium pump.

Acetylcholine↗
PubMed1960

The effects of acetylcholine on the turnover of phosphatidic acid and phosphoinositide in sympathetic ganglia, and in various parts of the central nervous system in vitro.

The effect of acetylcholine on the incorporation of P(32) into the individual phosphatides in slices of various structures of the nervous system has been studied. There was a marked stimulation of P(32) incorporation into phosphoinositide and phosphatidic acid, but not into phosphatidyl choline and phosphatidyl ethanolamine, in the cat stellate and celiac ganglia in vitro. Acetylcholine stimulated P(32) incorporation into certain phosphatides, primarily phosphoinositide and phosphatidic acid, in several structures of the cat and guinea pig brain; there was little or no effect of acetylcholine on phosphatide turnover in the inferior corpora quadrigsemina and cerebellar cortex. The suggestion is made that the phospholipid effect can best be explained as being concerned with the active transport of sodium ions out of the cell across the postsynaptic membrane of cholinergic neurons in response to acetylcholine.

Acetylcholine↗
PubMed1959

Phospholipide turnover in microsomal membranes of the pancreas during enzyme secretion.

After incubation of pigeon pancreas slices with P(32) and isolation of various fractions by differential centrifugation the deoxycholate extract of the microsome fraction was found to account for over half of the phospholipide P and over half of the P(32) incorporated into the phospholipides. The remaining phospholipide P and P(32) were fairly evenly distributed in the nuclei, zymogen granules, mitochondria, microsomal ribonucleoprotein particles, and the soluble fraction. When enzyme secretion was stimulated with acetylcholine about two-thirds of the increment in radioactivity in the total phospholipides was found in deoxycholate soluble components of the microsome fraction. The remainder of the increment was distributed in the other fractions. This indicates that the cellular component in which the increase in phospholipide turnover occurs on stimulation of secretion is a membranous structure. Evidence is presented which indicates that the increment in radioactivity in the non-microsomal fractions on stimulation of secretion is due to contamination of these fractions with fragments of the stimulated membranous structure. The distribution of P(32) radioactivity in each of the chromatographically separated phospholipides in the various fractions from unstimulated tissue paralleled the distribution of radioactivity in the total phospholipide fraction, indicating that individual phospholipides are not concentrated in different fractions but are associated together in the membranous structures of the microsome fraction. The major proportion of the stimulation of the turnover of the individual phospholipides also occurred in the microsome fraction. The distribution of radioactivity from glycerol-1-C(14) in the total phospholipides and in the individual phospholipides in the various fractions was similar to the distribution of P(32). In the microsome fraction acetylcholine stimulated the incorporation of glycerol-1-C(14) in each phospholipide which showed a stimulation of P(32) incorporation. The significance of the turnover of phosphatides in microsomal membranes in relation to the mechanism of secretion is discussed.

Acetylcholine↗