acid-phosphatase has been researched along with Adrenal-Cortex-Neoplasms* in 4 studies
4 other study(ies) available for acid-phosphatase and Adrenal-Cortex-Neoplasms
Article | Year |
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A case of testosterone-secreting adrenal cortical adenoma with spironolactone body-like inclusion.
Testosterone-secreting adrenal adenoma is rare. We recently experienced a 17-year-old pubertal girl who showed signs of virilization and a high serum level of testosterone. The excised adrenal gland showed a 3.5 x 3 x 3-cm cortical adenoma. Light and electron microscopic findings together with the high serum level and high tumor tissue contents of testosterone and dehydroepiandrosterone (DHA) indicated that the tumor was a testosterone-secreting adrenal cortical adenoma. This appears to be a rather rare tumor from a review of the literature. Interestingly, in this case, the cytoplasm of the tumor cells contained structures resembling spironolactone bodies. From the results of enzyme histochemistry, the steroidogenetic pathways in this tumor were speculated. Topics: Acid Phosphatase; Adenoma; Adolescent; Adrenal Cortex Neoplasms; Female; Histocytochemistry; Humans; Hydroxysteroid Dehydrogenases; Inclusion Bodies; Microscopy, Electron; Spironolactone; Testosterone | 1990 |
The effects of ACTH on acid phosphatase activity in endosomes, GERL and lysosomes of cultured adrenal tumor cells.
Cultured cells derived from a mouse adrenocortical tumor transplant are unspecialized in appearance, but produce basal levels of steroids and demonstrate a near-immediate steroidogenic response to ACTH. There is biochemical evidence that ACTH induces increases in the uptake of serum lipoproteins by these cells and that this material is hydrolyzed in lysosomes to free cholesterol, a precursor for steroid end products. To investigate morphologically the role of lysosomes in the steroidogenic activity of these cells, cultures were incubated for 4 h with and without ACTH, then processed for the ultrastructural localization of acid phosphatase (ACPase), a marker enzyme for lysosomes, and for GERL, the lysosome-forming subcompartment of the Golgi, and examined by TEM and HVEM. Steroid output was determined by a fluorometric technique. Unstimulated cells secreted basal levels of steroids. By TEM, large endosomes, some containing semi-compact material and ACPase reaction product, were occasionally seen at the cell periphery and in the Golgi region. The Golgi and GERL were poorly developed. Residual bodies, a few of them ACPase+, appeared in the Golgi region and in microtubule-associated clusters near the cell membrane. ACTH-stimulated cells secreted steroids at 8-10 fold basal values. In TEM records, they displayed numerous ACPase+ endosomes between the cell periphery and the Golgi. The Golgi and GERL regions appeared to be hypertrophied and many large, inclusion-containing, strongly ACPase+ residual bodies appeared here and in elongated microtubule-containing cell processes. HVEM micrographs showed more definitively that ACTH produced distinct increases in the size of GERL and in the number of ACPase+ organelles. Our results suggest that in unstimulated cells, endosomes, presumably containing media-derived material, gain lysosomal enzymes in or near GERL, are transformed to residual bodies as their contents are hydrolyzed, and are subsequently translocated by microtubules to the cell periphery for exocytosis. ACTH appears to intensify all of these effects. The "giant" lysosomes seen in stimulated cells may result from a fusion of smaller lysosomes. Their amorphous contents may reflect an inefficient hydrolysis of LDL to free cholesterol. Topics: Acid Phosphatase; Adrenal Cortex Neoplasms; Adrenocorticotropic Hormone; Cytoplasmic Granules; Golgi Apparatus; Histocytochemistry; Humans; Kinetics; Lysosomes; Microscopy, Electron | 1986 |
Enzyme histo-cytochemical studies in human adrenocortical adenomas. [II] Cushing's syndrome.
Enzyme histo-cytochemical staining was performed for 3 beta-hydroxysteroid dehydrogenase, alkaline phosphatase and acid phosphatase in the compact and clear cells of the adrenocortical adenomas associated with Cushing's syndrome (Cushing's adenomas). In the compact cells, enzymatic activities of 3 beta-hydroxysteroid dehydrogenase and alkaline phosphatase were stronger than those in the clear cells. Electron microscopic localization of alkaline phosphatase was mostly present on well developed microvilli, while, acid phosphatase was observed in lysosomes near the well developed smooth endoplasmic reticula. On the other hand, in the clear cells, cytochemical localization of alkaline phosphatase was mainly present on the intercellular plasma membrane, while acid phosphatase was mostly observed near the lipid droplets. Based on these data, functional aspects of the compact and clear cells in Cushing's adenomas are discussed. Topics: 3-Hydroxysteroid Dehydrogenases; Acid Phosphatase; Adenoma; Adrenal Cortex Neoplasms; Adrenocorticotropic Hormone; Adult; Alkaline Phosphatase; Cushing Syndrome; Female; Histocytochemistry; Humans; Middle Aged | 1983 |
Enzyme histocytochemical studies in human adrenocortical adenomas. [I]. Primary aldosteronism.
Enzyme histocytochemical staining including alkaline phosphatase, acid phosphatase, 3 beta hydroxysteroid dehydrogenase and 11 beta hydroxysteroid dehydrogenase was studied in human adrenocortical adenomas associated with primary aldosteronism. Histochemically, these enzyme activities were weaker in clear cell type adenomas than in the normal human adrenal cortex. While compact cell type adenomas showed stronger enzyme activities than the clear cell type adenomas. Electron microscopic localization of alkaline phosphatase was mainly observed in plasma membrane at the intercellular sites. Occasionally, this enzyme activity was also observed in the mitochondrial outer membrane, mainly in compact cells. The significance of these enzymes in the adenoma cells is discussed. Topics: 3-Hydroxysteroid Dehydrogenases; Acid Phosphatase; Adenoma; Adrenal Cortex Neoplasms; Adult; Alkaline Phosphatase; Female; Histocytochemistry; Humans; Hyperaldosteronism; Male; Middle Aged | 1983 |