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After administering 1-DOPA for 7 d a decreased number of secretory granules as well as pronounced rough endoplasmic reticulum and Golgi apparatus were noted in C cells. A single dose of 1-DOPA did not inhibit C cell stimulation induced by a single dose of calcium gluconate. On the other hand, parallel administration of alpha-methyl-DOPA and calcium gluconate did not decrease the number of C cell secretory granules, which were observed after administration of calcium gluconate alone. The data suggest that the presence of DOPAmine (formed the 1-DOPA) in the secretory granules is a prerequisite for normal functioning of secretory processes in thyroid C cells.
Based on morphological and histochemical data, the Authors describe the distribution of "EC" (5-HT-producing) and of the other endocrine cells of the "APUD" series (polypeptide hormone-producing) in the gastro intestinal tract of weaned and unweaned 3-4 month old calves. The results demonstrate that: -- no difference concerning the different diet can be correlated; -- no endocrine cell is present in the vorestomachs; -- the "EC" cells in the abomasum prevail in the fundus glands; they are demonstrable also in every tract of the intestine and are more numerous in the duodenum and in the rectum; -- within the "APUD" series four cellular types are demonstrable in the abomasum; two are in the cardias, one in the fundus and one in the pylorus glands; the last one probably corresponds to the gastrin-producing "G" cells. -- In the small intestine, particularly numerous in the duodenum, a probably heterogeneous family of endocrine cells is present, while in the coecum, in the colon and, above all, in the rectum, cells probably corresponding to "EG" cells are identifiable. These results are compared to those previously obtained in the adult Cattle: remarkable differences are demonstrable only within "APUD" cells of abomasum.
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The amine precursor uptake and decarboxylation (APUD) system of cells has been claimed to derive from the embryological neural crest. This assertion has been uncritically accepted. There is much contradictory evidence, especially about the origin of the gastrointestinal and respiratory APUD cells. There is further evidence that the embryological derivation of a particular cell does not relate to the possibility of ectopic peptide hormone synthesis by malignant tumours arising from that cell type. There are many reports of APUD activity by endodermally and mesodermally derived tumours, and of "APUDomas" with endodermal microscopic features. It seems that the concept of dedifferentiation explains the observed data much more satisfactorily and that the presence of double minute chromosomes may denote gene amplification and cellular production of peptides.
Animals with experimental uremia, which underwent thyroparathyroidectomy, reveal numerous metabolic disorders that can influence morphology and activity of endocrine cells of the scattered neuroendocrine system. The aim of the study was the evaluation of the influence of thyroparathyroidectomy in rats with chronic renal failure on APUD system cells localized in the respiratory tract. The examination was conducted on the group of 20 rats. Thyroparathyroidectomy was performed 30 days after nephrectomy. Fragments of the lungs and trachea were collected 14 days after the operation. Routinely prepared paraffin sections were stained with H+E and with silver method. The immunohistochemical reactions were conducted with the use of antibodies against calcitonin (CT), synaptophysin (SPh), somatostatine (ST), and neuron-specific enolase (NSE) The results were estimated in light microscope on the basis of stain reaction of endocrine cells. Our examination showed that chronic renal failure affects the functioning of endocrine cells. We also observed the increase in APUD system cell number in the trachea and the lungs after thyroparathyroidectomy in uremic rats.
A 27 year old woman had in 1965, a paraneoplastic Cushing's syndrome was cured by removal of a pulmonary tumour. The case was published in June 1968. After a normal pregnancy, a recurrence of the Cushing's syndrome in 1969 led in 1970 to bilateral total adrenalectomy in two stages. Pathology showed hyperplastic adrenal glands. After 11 years follow up, we have not noted any relapse of the tumour nor of the Cushing's syndrome. The pathological appearance of the lung carcinoma removed in 1965 (endocrinoid or neuroid structures) suggests that this was an "apudoma" and that the recurrence of the Cushing's syndrome was perhaps an "apudomatosis" involving the pituitary ACTH cells.
Disturbances in renal homeostatic function lead to changes in endocrine cell secretory activity. The aim of this study was the histomorphological estimation of dependence of gastric APUD system cell morphology and function on the time after subtotal nephrectomy in Wistar rats. Fragments of gastric pylorus were collected 1. 2, 4, and 6 weeks after nephrectomy. Paraffin sections were stained with H+E and by silver impregnation. Immunohistochemical reactions with the use of specific antibodies against calcitonin gene-related peptide (CGRP), synaptophysin (SPh). somatostatin (ST), and neuron-specific enolase (NSE) were also performed. Immunoreactivity of the examined substances in the pyloric mucosa in the first week after nephrectomy was lower than in the control group. However, in the following time intervals, endocrine cells showed stronger immunostaining in comparison with the control rats. The results suggest that chronic renal failure can modulate secretory activity of APUD system cells.
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The paper presents the latest opinions dealing with biological features (the hormone production) and histogenesis of the small cell lung cancer (SCLC). The authors try to explain the problem of the rapid progression of SCLC as well as the rapid insensitivity to radiation and chemotherapy following initial responsiveness of SCLC.
We report the metastasis of a rectal carcinoid to the dura mater of the posterior fossa. The clinical presentation was unusual because of a 10-year latent period between resection of the primary rectal tumor and symptoms and signs of the posterior fossa metastasis; the radiological findings were atypical of a metastasis. Gastrointestinal carcinoids, apudomas, and the concept of the APUD endocrine cell family are reviewed.
The complete thyroid and parathyroid gland removal leads to the abrupt reduction of calcitonin, which can be a factor stimulating growth and intensified activity of APUD system cells in the respiratory tract. Thus, neuroendocrine cells in the lungs and trachea in rats after thyroid and parathyroid removal were evaluated. Paraffin specimens of the examined organs were stained with H+E and impregnated with silver. Calcitonin, synaptophysin, somatostatin, and neuronal-specific enolase were detected immunohistochemically by the use of rabbit specific antibodies. Antibodies used in the study immunostained neuroendocrine cells of the examined organs. Rats with removed thyroid and parathyroid glands presented weakened reaction compared to the control group.
The case of a 40-year-old woman with primary small cell carcinoma of the cervix is reported. She developed widespread metastates and florid Cushing's syndrome. Serum ACTH levels were greatly elevated and no site of production other than the tumor could be demonstrated at autopsy. The tumor cells demonstrated features characteristic of cells of the APUD series. Such cells have been demonstrated in normal cervical epithelium; it is likely that they may become malignant, giving rise to tumors with a potential to secrete polypeptide hormones. This case suggests that endocrine active "Apudomas" may arise from the uterine cervix. Certainly, patients with small cell carcinoma of the cervix should be investigated with appropriate serum assays for polypeptide hormones.
Historically, the enterochromaffin cell was the first endocrine cell type detected in avian gut; subsequently, a number of types of such cells were distinguished on the basis of the ultrastructural features of the secretory granules. More recently, immunocytochemical procedures have revealed somatostatin-, pancreatic polypeptide (PP)-, polypeptide YY-, glucagon-, secretin-, vasoactive intestinal peptide (VIP)-, gastrin-, cholecystokinin-, neurotensin-, bombesin-, substance P-, enkephalin-, motilin-, and FMRFamide-like immunoreactivity in avian gastrointestinal endocrine cells. Most endocrine cells are located in the antrum; there are a number in the proventriculus and small intestine but few in the gizzard, cecum, and rectum. Several avian gastroenteropancreatic hormones, including glucagon, VIP, secretin, bombesin, neurotensin, and PP, have been isolated and sequenced. They resemble the equivalent mammalian peptides in terms of molecular size but differ in amino acid composition and sequence; some (e.g., VIP) differ only in minor respects, others (e.g., secretin) more radically. Gastrointestinal endocrine cells appear late in development; available data indicate that few types are recognized by either immunocytochemistry or electron microscopy before 16 days of incubation. Experimental evidence has shown that at least the majority of gut endocrine cells are of endodermal origin and are not derived from the neural crest or neuroectoderm as earlier proposed. In early embryos, the progenitors of gastrointestinal endocrine cells are more widespread than are the differentiated cells in chicks at hatching. This, along with other observations, raises the question of factors that might influence the differentiation of gut endocrine cells.
Four cases of malignant colonic tumors diagnosed by light microscopy as "small cell undifferentiated carcinomas" were shown by electron microscopy to have neurosecretory-type granules. Biochemical analysis of tumor tissue extracts disclosed the presence of considerable levels of VMA and catecholamines in all tumors; 5-HIAA was present in one tumor. Clinically, there had been no signs or symptoms attributable to those or related substances. Similar observations have been reported in a variety of neuroendocrine neoplasms; for example, the demonstration of neurosecretory-type granules and determination of amine or peptide materials in tumor tissue or body fluids may not be necessarily reflected in clinical hormonal syndromes or obvious metabolic abnormalities. Our structural and biochemical observations indicate that, regardless of clinically evident hormonal activity or lack thereof, some small cell "undifferentiated" colonic cancers derive from APUD elements, and therefore they should be classified within the group of neuroendocrine carcinomas. The evident secretory capabilities of these carcinomas suggest obvious diagnostic possibilities and could conceivably lead to a reappraisal of current therapy.
Somatostatin is released in the blood, in synaptic clefts, and in the intercellular space in response to a variety of stimuli. In view of its multiple functions, various sites of synthesis and release, and rapid inactivation, as well as extremely low levels of somatostatin in the peripheral blood, somatostatin can hardly be considered to be a hormone whose target is reached via the general circulation. The target organs of cells may be located near the somatostatin-producing cells and can be reached via local circulation such as the hypophyseal portal system and the microportal circulation in the gut mucous membrane. Somatostatin released from the neurons acts as a hypophyseotropic hormone and a neurotransmitter or neuromodulator. Furthermore, somatostatin may also act in a paracrine fashion by being released into the intercellular space. This space may sometimes be compartmentalized by tight junctions so that the action of the peptide is limited only to the adjacent cells. In this fashion, the pancreatic islet somatostatin influences nearby A- and B- cell activities. Gut D cells, prototypes of APUD or paraneuron cells, show considerable similarity to neurosecretory cells not only in biochemical processes but also morphologically. While the somatostatin neurons in the brain respond to dopaminergic and catecholaminergic agonists, D cells in the gut respond to chemical stimuli in the lumen by sensing them with microvilli. They release somatostatin into the blood stream, into the intercellular space, and into the gastric and intestinal lumen. Luminal somatostatin may affect other endocrine and nonendocrine cells in the mucous membrane of the gut. It is noted that the same stimulatory agent does not always stimulate somatostatin release from different organs; one agent stimulates the release from one organ and suppresses release from the other organ.