Increase In Ribosomes Research Articles

Histochemical and ultrastructural investigation on the endocrine cells of the stomach in hypersecreting (pylorus-ligated) rats.

To get new information on the patho-physiology of the endocrine cells of the gastric mucosa and to investigate their role in the gastric secretion, an histochemical and electronmicroscopical investigation has been undertaken during experimental acute gastric hypersecretion induced in rats by pyloric ligation (Shay rats). Of the various types of endocrine cells, the ECL (entero-chromaffine-like) cells of the fundic mucosa showed ultrastructural evidences of marked activity (partial degranulation, formation of pro-granules, increase in ribosomes and enlargement of the rough endoplasmic reticulum). By histochemical techniques, cells interpreted as ECL cells showed a progressive decrease in argyrophilia, dopamine storage after L-DOPA administration, and histamine content. Other cell types, such as the A-like and EC cells were apparently unaffected. The antral G cells appeared, in the electron microscope, to be fully granulated and therefore probably inactive. It is concluded that, during hypersecretion in pylorus-ligated rats: Since the gastric hypersecretion in Shay rats is believed to be due to a vagal reflex, it can be suggested that the ECL cells, probably under a vagal control, play a role in the gastric secretion.

Anoxic-ischaemic cell change in rat brain light microscopic and fine-structural observations

Anoxic-ischaemic neuronal damage has been defined by a combined light and electron microscope study of the neocortex and hippocampus of rats exposed to nitrogen intermittently during a period of 40 min with (“Levine preparation”) and without (“nitrogen only” animals) interruption of blood flow in the right common carotid artery. The animals were killed by perfusion-fixation with glutaraldehyde after survivals (measured from the end of exposure to nitrogen) of 45 min to 2 hr. Microvacuolation, the earliest stage of anoxic-ischaemic neuronal damage, and ischaemic cell change were observed in the neocortex and hippocampus of both groups of animals while ischaemic cell change with incrustations was confined to the neocortex. Ultrastructural examination showed that the majority of microvacuoles in the neuronal cytoplasm correspond to swollen mitochondria. Dilatations of both smooth and granular endoplasmic reticulum accompanied the mitochondrial swelling. There was an associated apparent increase in ribosomes and in cytoplasmic matrix density. The evolution of ischaemic cell change with an without incrustations appeared to occur by a progressive condensation of the cytoplasm between all intraneuronal dilated spaces, sometimes accompanied by shrinkage of the swollen mitochondria. Surface irregularities and the apparent isolation of dense areas of the neuronal soma by areas of lesser electron density appeared to represent the incrustations of light microscopy. Swollen astrocytic processes surrounded the damaged neurones at all stages of the cell change. Ultrastructural changes occurring in axon terminals and dendrites are described.

Hormone-Dependent Accumulation of Rough Endoplasmic Reticulum in Mouse Mammary Epithelial Cells <italic>In Vitro</italic><xref ref-type="fn" rid="FN1">1</xref>

Abstract Mammary epithelial cell differentiation, as effected by the interplay of insulin, corticosteroid(s), and prolactin, has been further studied in vitro. Emphasis has been placed on the synthesis of casein in relation to the fabrication and function of the rough endoplasmic reticulum (RER). Minimal hormone requirements for the accumulation of the RER are insulin and corticosteroid. This is based on determinations of membrane-linked NADH-cytochrome c reductase (EC 1.6.99.3) and of RNA content of isolated RER. Accumulation of the enzyme is affected very little by insulin, modestly increased by hydrocortisone, and greatly enhanced by the combination of the two hormones. RNA content of RER is virtually unaltered by hydrocortisone, but is increased by insulin. This effect of insulin is, however, enhanced by the presence of hydrocortisone. Addition of hydrocortisone to an insulin-containing postmitotic system causes redistribution of free ribosomes to the membrane-bound variety without a net increase in ribosomes. In the absence of the steroid, insulin promotes development of an unstable RER which also is deficient in NADH-cytochrome c reductase. Prolactin does not affect the membrane-linked enzyme. It does, however, stimulate the rate of RNA synthesis and increases the RNA content of the membrane system. In the absence of RER, prolactin also increases the rate of RNA synthesis, but this effect is not sustained. Three lines of evidence strongly suggest that casein formation by these epithelial cells is dependent upon the presence of the RER that is induced by insulin and hydrocortisone. (a) There is close agreement between casein synthesis and RER formation as a function of hydrocortisone concentration. (b) RER formation precedes casein synthesis. (c) Casein formation requires sustained stimulation of RNA synthesis by prolactin, which, in turn, is dependent on the presence of RER.

Electron microscopic studies on the adrenal medulla and adrenal cortex of hypertensive rats. 2. Experimental hypertensive rats.

DOCA hypertension, renal hypertension, and cerebral hypertension were induced in Wistar rats. In the acute and chronic stages, noradrenaline storing cells of the adrenal medulla and cells of the zona fasciculata in the adrenal cortex were studied, both electron microscopically and histometrically, in order to compare them with their respective controls. 1. (a) In the acute stage of DOCA hypertension, (i) the number of noradrenaline storing granules was not different from that in the controls. Vesicles were about 1.6 times as numerous as those in the controls. Some of the granules and vesicles varied greatly in size. However, only a few of them probably representing initial secretory granules were noted. (ii) A large number of relatively large secretory granules of moderate electron density were found within the cytoplasm of cells of the zona fasciculata of the adrenal cortex. Both the number of the mitochondria and the number of ribosomes were decreased. (b) In the chronic stage of DOCA hypertension, (i) the nor-adrenaline storing granules and vesicles showed findings similar to those described in the acute stage. Especially noted were giant granules and vesicles. (ii) Cells of the zona fasciculata of the adrenal cortex also gave findings similar to those in the acute stage. 2. (a) In the acute stage of renal hypertension, (i) the number of noradrenaline storing granules was not significantly different from the controls. The number of vesicles was 1.7 times as great as that of the controls. Granules and vesicles varied in size and small ones were also found in abundance. (ii) In the cells of the zona fasciculata of the adrenal cortex, secretory granules probably representing lipid droplets were also found to be rather abundant as compared with controls. (b) In the chronic stage of renal hypertension, (i) no remarkable changes were noted in the number of noradrenaline storing granules and vesicles. Morphological changes were not remarkable except for slightly larger vesicles than those in the controls. (ii) In the cells of the zona fasciculata of the adrenal cortex, there were more abundant round secretory granules of moderate electron density than those in the controls. Dilatation and an increase of smooth-surfaced endoplasmic reticulum and ribosomes were noted. 3. (a) In the acute stage of cerebral hypertension, (i) the number of noradrenaline storing granules was unchanged and the number of vesicles was about 1.9 times that of the controls. As to the morphology, both granules and vesicles were larger than the controls. (ii) In the cells of the zona fasciculata of the adrenal cortex, large secretory granules of low electron density probably representing lipids were noted. Dilatation and an increase of smooth-surfaced endoplasmic reticulum and an increase of ribosomes were noted. (b) In the chronic stage of cerebral hypertension, (i) noradrenaline storing granules were increased (1.2 times those in the controls) and vesicles were also found abundantly (2.6 times those in the controls). Both granules and vesicles were variable in size and there were abundant small granules as well. (ii) In the cells of the zona fasciculata of the adrenal cortex, secretory granules of medium electron density probably representing lipids were found to be abundant. The smooth-surfaced endoplasmic reticula were di-

Hormone-dependent Accumulation of Rough Endoplasmic Reticulum in Mouse Mammary Epithelial Cells in Vitro

Abstract Mammary epithelial cell differentiation, as effected by the interplay of insulin, corticosteroid(s), and prolactin, has been further studied in vitro. Emphasis has been placed on the synthesis of casein in relation to the fabrication and function of the rough endoplasmic reticulum (RER). Minimal hormone requirements for the accumulation of the RER are insulin and corticosteroid. This is based on determinations of membrane-linked NADH-cytochrome c reductase (EC 1.6.99.3) and of RNA content of isolated RER. Accumulation of the enzyme is affected very little by insulin, modestly increased by hydrocortisone, and greatly enhanced by the combination of the two hormones. RNA content of RER is virtually unaltered by hydrocortisone, but is increased by insulin. This effect of insulin is, however, enhanced by the presence of hydrocortisone. Addition of hydrocortisone to an insulin-containing postmitotic system causes redistribution of free ribosomes to the membrane-bound variety without a net increase in ribosomes. In the absence of the steroid, insulin promotes development of an unstable RER which also is deficient in NADH-cytochrome c reductase. Prolactin does not affect the membrane-linked enzyme. It does, however, stimulate the rate of RNA synthesis and increases the RNA content of the membrane system. In the absence of RER, prolactin also increases the rate of RNA synthesis, but this effect is not sustained. Three lines of evidence strongly suggest that casein formation by these epithelial cells is dependent upon the presence of the RER that is induced by insulin and hydrocortisone. (a) There is close agreement between casein synthesis and RER formation as a function of hydrocortisone concentration. (b) RER formation precedes casein synthesis. (c) Casein formation requires sustained stimulation of RNA synthesis by prolactin, which, in turn, is dependent on the presence of RER.

The Localization of Phorbol Ester 14C Acetate in Papillomas that Were Initiated With 7,12 Dmba and Promoted with Phorbol Ester an Electron Microscopic Autoradiography Study

Phorbol ester acetate was produced by the esterification of the free hydroxyl of phorbol ester C (the tumor promoting agent from croton oil). The phorbol ester acetate was used to promote skin tumors in female mice that had previously received a subcarcinogenic dosage of 7,12 DMBA. The morphology of the tumor revealed an epidermal hyperplasia as well as a hyperkeratosis of the stratum corneum. There was a marked increase in the intercellular space in the strata basale and spinosum. These cells also demonstrated an increase in ribosomes and polysomes. Many of the mitochondria of these cells revealed intramitochondrial granules that resembled lipid droplets. Phorbol ester- 14 C acetate was prepared by acetyl-2- 14 C esterification of the free hydroxyl of the phorbol ester C. The phorbol ester- 14 C acetate was applied to papillomas that were initiated with 7,12 DMBA and promoted with phorbol ester acetate for 90 days. Grains due to the phorbol ester- 14 C acetate were observed overlying the loose chromatin of the nuclei and tonofibrils.

A combined light and electron microscope study of early anoxic-ischaemic cell change in rat brain

Summary Anoxic-ischaemic neuronal damage was studied by a combined light and electron microscope study of the brains of 4 rats exposed to nitrogen intermittently during a period of 40 min after interruption of blood flow in the right common carotid artery (‘Levine preparation’). The animals were killed by perfusion-fixation with glutaraldehyde after survival of 1 h (measured from the end of exposure to nitrogen). Microvacuolation, the earliest alteration, was abundant in the ipsilateral hippocampi (h1) of two animals. The electron microscope study was restricted to this region. Microvacuoles in paraffin and plastic sections (light microscope) appeared as apparently empty circular spaces (0.16–2.5 μm in diameter) in the cytoplasm. At the ultrastructural level most microvacuoles were seen to be swollen mitochondria retaining their double membranes despite progressive disruption of their internal structure. Dilatations of the tubules, vesicles and cisternae of the endoplasmic reticulum were also observed. There was an associated apparent increase in ribosomes and in cytoplasmic matrix density. The damaged neurones were surrounded by swollen astrocytic processes.

In vitro effects of the nerve growth factor on the fine structure of the sensory nerve cells

Dorsal root ganglia from 8-day chick embryos were explanted in semisolid media with or without a specific nerve growth factor (NGF). The ganglia were incubated for a period of 4 and 12 h and examined with the electron microscope. The presence of the NGF in the culture medium calls forth striking and rapid changes in the fine structure of the neurons. The nuclei develop an irregular contour and denser clumped chromatin in comparison with the controls. In the cytoplasm the Golgi apparatus is dilated; in some cells there is a massive increase in ribosomes associated with increased number of membranous elements of endoplasmic reticulum. Neurofilaments and neurotubules, sparse in control cultures, are already prominent after 4 h of incubation in the presence of the NGF. After 12 h, the cytoplasm of most ganglionic cells is packed with large masses of neurofilaments.

Ultrastructure of vaginal keratinization in estrogen treated immature BALB/cCRGL mice.

In 10-day-old Balb/cCrgl mice, the subcutaneous injection of 0.1 μg of estradiol in distilled water per animal per day resulted in the conversion, over a 4 day period, of the original 3 cell layered cuboidal epithelium to a stratified, multilayered, fully keratinized epithelium. By light microscopy, there was development of a prominent stratum germinativum and of a mucinified surface on the 1st day, followed by the sequential formation of a stratum spinosum, a stratum granulosum, and a stratum corneum. By electron microscopy, the principal early modifications consisted of a marked increase in ribosomes, desmosomes, and 70 A cytoplasmic filaments, the latter being aggregated into approximately 700 A fibrils. The subsequent establishment of a keratin layer was preceded by the appearance of keratohyaline granules and the disappearance of mitochondria and endoplasmic reticulum in cells immediately above the stratum spinosum and by the development of a transitional cell layer in which there was progressive aggregation of cytoplasmic filaments and disappearance of nuclei, keratohyaline granules, and free ribosomes. In the upper stratum granulosum, transitional cell layer, and stratum corneum there were distinctive modifications in desmosomal structure (composite and modified desmosomes). The morphological and physiological significance of these observations is discussed.

EFFECT OF THIOACETAMIDE-INDUCED SUBLETHAL HEPATIC CELL INJURY ON PROTEIN SYNTHESIS.

SummaryElectron microscopic and radiochemical studies were performed in mild sublethal hepatic cell injury (cloudy swelling) produced by small peroral doses of thioacetamide. Azurophilia, ribosomes and polyribosomes decreased or disappeared in injured cells at 5 1/2 hours. At 48 hours the cells in the outer portion of the lobule contained a marked increase in ribosomes and polyribosomes, while centrally located cells continued to show evidence of the earlier injury. At 5 1/2 hours after thioacetamide there was a decreased uptake of the label from administered C14-L-leucine in serum albumin and in total hepatic protein while it was increased in the hepatic RNA-protein. These findings were interpreted to indicate that incorporation of amino acid into hepatic RNA-protein is not measurably impaired by mild injury due to thioacetamide, but that synthesis or secretion of serum albumin is impaired. At 48 hours, amino acid incorporation in total hepatic protein was decreased in thioacetamide treated animals, but ...