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Biomedical subjects

J N Loeb

Publications and source records attributed to J N Loeb.

At least 55 records · Page 3Linked to original sources
PubMed1975

Scanning electron microscopy of glucocrticoid-treated hepatocytes and hepatoma cells in culture.

The morphological effects of exposure to hydrocortisone have been examined in two cell lines of liver origin by scanning electon microscopy. In one of these, an aneuploid line derived from a Morris hepatoma, the presence of hormone results not only in a suppression of cell proliferation, but in a marked flattening of the cells and loss of surface microvilli; in the other cell line, a diploid line derived from adult rat liver, the suppression of cell division is less marked, and the morphological effects of the hormone are far less striking. While the suppression of cell division in both of these cell lines is known to be rapidly reversible upon the removal of hormone, the presence of hormone causes the hepatoma cells to assume both monolayer growth characteristics and a morphology resembling those of cells derived from normal liver.

Animals↗
PubMed1974

Properties of plasminogen activators formed by neoplastic human cell cultures.

A series of human cell lines has been examined for fibrinolysis in culture. The sera that are activating for fibrinolysis by human cells are mouse, monkey, human, horse, and bovine. Individual human sera show considerable variation in the ability to activate fibrinolysis. In common with other neoplastic or transformed mammalian and avian cell cultures, human cell lines of neoplastic origin produce substantial amounts of plasminogen activator. Several cultures of nonmalignant origin also produce plasminogen activator, whereas cultures obtained from trypsinized human embryos, or from human embryonic skin do not. The human melanoma plasminogen activators are of two kinds: a major component with a mol wt of 50,000, and a minor species with a mol wt of approximately 60,000. Both are DFP sensitive, serine proteases.

Animals↗
PubMed1973

Suppression of DNA synthesis in hepatoma cells exposed to glucocorticoid hormone in vitro.

Glucocorticoid hormone is shown to markedly suppress DNA synthesis in a line of rat hepatoma cells in vitro. In the presence of 300 nM hydrocortisone or 30 nM dexamethasone the incorporation of radioactive thymidine falls to 50% of control levels by 36 hr, and at higher concentrations of hormone inhibition can be noted as early as 12 hr and is nearly complete by 24 hr. This inhibition of radioactive thymidine incorporation reflects a true suppression of DNA synthesis, is accompanied by a corresponding inhibition of cell proliferation, and is readily reversible upon subsequent removal of hormone. In contrast to previously described effects of the glucocorticoid hormones on various cells of lymphoid origin, the inhibition of DNA synthesis in these hepatoma cells is not accompanied by appreciable cell lysis or by degradation of preformed DNA, and even when [(3)H]thymidine incorporation into DNA is inhibited by 90% or more, incorporation of [(14)C]uridine into RNA proceeds with little change. These findings all parallel previous observations on the effects of glucocorticoid hormone on the livers of intact animals and suggest that studies on the mechanism of the inhibition of DNA synthesis in the present more isolated system may lead to a better understanding of the means by which these compounds inhibit liver growth in vivo. Despite the ready suppressibility of DNA synthesis in these hepatoma cells and in two other cell lines of liver origin, none of these cell lines was found to be inducible for tyrosine aminotransferase. The apparent dissociation between two "steroid-sensitive" phenomena is of interest and warrants further investigation.

Animals↗
PubMed1972

Effects of cortisone administration on rat liver mitochondria. Support for the concept of mitochondrial fusion.

The present studies investigate the basis for the marked increase in mitochondrial size and approximately reciprocal decrease in mitochondrial number which have been observed in the livers of rats treated with cortisone acetate. Comparisons of the content and specific activity of mitochondrial DNA in the livers of control and cortisone-treated animals prelabeled with radioactive thymidine support the possibility that these changes in mitochondrial size and number are the result of a process of mitochondrial fusion. A consideration of various conditions now known to result in the formation of large mitochondria in other systems suggests that interference with mitochondrial respiration may provide a stimulus for such a process. The biochemical approach described in the present study may prove useful in investigating the origin of large mitochondria in other systems as well.

Animals↗
PubMed1970

Sedimentation properties of rat liver mitochondria. Effects of cortisone treatment.

A prediction of the velocity of sedimentation of rat liver mitochondria in sucrose gradients is made on the basis of recent measurements of the size of isolated mitochondria suspended in sucrose medium and the model proposed by Bentzel and Solomon to describe the osmotic behavior of mitochondria. The experimentally observed velocity is extremely close to the predicted value and confirms by a different approach the estimate of mitochondrial volume made by Baudhuin and Berthet on the basis of electron microscopic measurements. Because cortisone treatment of rats is known to result in a marked increase in mitochondrial size as observed under the electron microscope, mitochondria were co-isolated from livers of control and cortisone-treated animals, and the sedimentation behavior of the mixtures was examined by sucrose density gradient centrifugation. Mitochondria from cortisone-treated animals were found to sediment 1.4 times as rapidly as those from control animals, indicating that their increased size cannot entirely be due to an increased imbibition of fluid from the surrounding sucrose medium, and that the change in size must at least in part be due to a change in content of nondiffusible mitochondrial components. Although the increase in sedimentation velocity of mitochondria from cortisone-treated animals is striking, it is less than that predicted solely on the basis of their size relative to that of control mitochondria. It is concluded that the increases in mitochondrial size and content of nondiffusible components produced by cortisone treatment are accompanied by alterations in mitochondrial composition as well.

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