Proliferation Of Endoplasmic Reticulum Research Articles

Development and Ultrastructure of Extrafloral Nectaries in Ancistrocactus scheeri (Cactaceae)

Extrafloral nectaries of Ancistrocactus scheeri appear to be modified spines because they are formed by an areole meristem, are unvascularized, and have no trichomes or stomata. The vascularized stalk of the gland is interpreted as a tubercle-derived outgrowth. Secretion is eccrine, and there is no proliferation of endoplasmic reticulum or dictyosomes. Stereological analysis did not reveal any quantitative changes in the gland as secretion was initiated, but there was some restructuring of cristae in the mitochondria. The relative volumes of organelles during secretion were: nuclei, 12.9% of cell volume; vacuoles, 24.3%; mitochondria, 8.23%; plastids, 4%; dictyosomes, 0.30%; and hyaloplasm, 50.2%.

Ultrastructure of the developing pigment strand of rice (Oryza sativa L.) in relation to its role in solute transport

The developing pigment strand of rice (Oryza sativa L.) was studied by conventional electron microscopy and also by use of thick sections post-fixed with zinc iodide and osmium (ZIO). When the rice caryopsis achieves maximum length, a suberised adcrusting wall layer is laid down over the original primary walls of the pigment strand. Concomitant with suberin deposition a proliferation of tubular endoplasmic reticulum occurs in the cytoplasm giving rise to numerous interconnected vesicles which bear ribosomes. The vesicles in the general cytoplasm retain their ribosomes while those close to the wall become smooth and contain an electron-opaque granular material which is eventually deposited to the outside of the plasmalemma. This granular material may be the precursor(s) from which suberin is polymerised. The suberised wall attains about six times the width of the original primary wall and plasmodesmata, which traverse both primary wall and suberised wall layers, become greatly elongated. Lipid bodies increase in both size and frequency during development, eventually coalescing to form a complete plug across the pigment strand and occluding the symplast of this tissue. The significance of these ultrastructural observations is discussed in relation to the previously demonstrated role of the pigment strand as a translocation pathway for water and assimilates during grain filling.

Hepatotoxicity of vitamin A and ethanol in the rat

To study the possible hepatotoxicity of vitamin A supplementation and its potentiation by ethanol, rats were fed diets with either normal or fivefold increased vitamin A content, both with or without ethanol. Ethanol with a normal vitamin A diet produced the expected proliferation of the smooth endoplasmic reticulum and moderate mitochondrial lesions. Vitamin A supplementation by itself produced endoplasmic reticulum proliferation, slight enlargement of mitochondria, and moderate decrease in cytochrome oxidase activity and cytochrome aa3 content. The combination of high vitamin A and ethanol resulted in much more striking lesions, with giant mitochondria containing paracrystalline inclusions and depression of oxygen consumption in state-3 respiration with five different substrates, including palmitate and palmitoyl coA. The depression of fatty acid oxidation may have contributed to the lipid accumulation. The blood levels of vitamin A were unaffected whereas liver levels of vitamin A were increased by vitamin A supplementation and decreased by ethanol. As a net result the liver vitamin A content of the high-A-ethanol group was not greater than that of the normal-A-control group, suggesting that a metabolite of vitamin A rather than vitamin A itself may have been responsible for the potentiation of vitamin A toxicity by ethanol. Mitochondrial toxicity reflected itself also in decreased content of various cytochromes and reduced activity of enzymes, including glutamate dehydrogenase. The activity of the latter was increased in the serum. Implications of these findings for the routine treatment of alcoholics with vitamin A and the monitoring for possible signs of toxicity are discussed.

Endoplasmic Reticulum Formation during Germination of Wheat Seeds

This study demonstrates germination-induced ultrastructural changes in wheat (Triticum aestivum L. cv Arthur) aleurone cells. Seeds imbided for 4 hours in water contained endoplasmic reticulum (ER) or ER-like membranes as vesicles or as short segments of membrane associated with the spherosomes on the periphery of aleurone grains. Aleurone cells incubated between 8 and 10 hours contained abundant ER membranes mainly associated with the nuclear envelope and, to a lesser extent, with the spherosomes surrounding the aleurone grain. The membranes located on the periphery of the nucleus occurred as regions of stacked cisternae. When aleurone cells were analyzed by morphometry, the increase in ER during incubation was found to be greater than 2-fold. During the same incubation period, other organelles did not change significantly. The early increase in ER was not affected by gibberellin incubation. Thus, the rapid proliferation of ER observed during the early stages of germination in aleurone cells of wheat is not likely to be controlled directly by gibberellin.

Chlordecone‐induced hepatic dysfunction

Chlordecone (Kepone) is a decachloroketone analog of the dodecachlorohydrocarbon mirex and is used as a stomach poison insecticide. Despite the structural similarity to mirex, chlordecone is unlike mirex in general organ-specific toxic properties. Chlordecone is primarily accumulated in the liver, where it causes a variety of morphological and biochemical alterations. Although less effective than mirex as a hepatotoxin, it causes liver enlargement, focal necrosis, mitochondrial changes, fatty infiltration of hepatocytes, and proliferation of endoplasmic reticulum. Chlordecone accumulation and morphological alterations in the liver were also observed in occupationally exposed human patients. Induction of hepatic microsomal mixed-function oxidases (MFOs) and impaired production and utilization of hepatocellular energy are the principal biochemical aberrations produced by chlordecone. Chronic exposure causes carcinogenesis in mice and rats. Hyperplastic nodules, which progress to hepatocellular carcinomas, are the principal pathological lesions. Acute and chronic exposures to chlordecone result in hepatobiliary dysfunction manifested as impaired excretion of anionic compounds accompanied by choleresis. Exposure to chlordecone results of greatly potentiated haloalkane hepatotoxicity, representing a most potent toxic interaction at otherwise individually nontoxic levels. In view of the demonstrated carcinogenic effect of chlordecone, such interactions at very low levels assume extraordinary significance in terms of chronic toxicological and pathological manifestations induced by combinations of toxic chemicals.

Morphogenesis of cerebellar lesions in bovine familial convulsions and ataxia.

Cerebellar lesions develop in a heritable disorder characterized by recurrent episodic seizures in newborn and young calves and by ataxia in survivors of several bouts of convulsions. Earliest changes were altered patterns of phosphatase reaction products in Purkinje cells. Purkinje cells axons in the outer half of the granular layer developed fusiform or spheroidal argyrophilic swellings. Early lesions were restricted to the lingula and uvula, but cases with more persistent clinical disease involved other parts of the vermis. In ataxic calves these lesions were also in the cerebellar hemispheres. The axonal swellings showed proliferation of tubulovesicular endoplasmic reticulum, neurofibrils and mitochondria. In other swellings axoplasm was degenerate, and in some it resembled Purkinje cell cytoplasm. In some clinically normal adult transmitters of the disorder, light microscopy showed some similar swellings, but most calves that recovered had no lesions.

Morphological changes of the kidney and bone of rats in chronic cadmium poisoning

Wistar rats were given drinking water containing 200 ppm CdCl 2 for 4 to 91 weeks and the kidneys and femoral bones were examined morphologically. Histological examination showed degenerative changes in the proximal convoluted tubules. Electron microscopically tubular changes consisted of cell edema, swelling of mitochondria, proliferation of smooth-surfaced endoplasmic reticulum, vacuolar degeneration, and coagulative necrosis. These alterations were observed to progress with increase of urinary excretion of protein and cadmium levels in the kidneys. Spontanous nephropathy was found more frequently in cadmium-exposed rats than in controls. The bones showed no significant change in histological and roentgenological examinations, as well as in assay of bone mineral content.

Experimental studies on insecticides commonly used in India.

Using hexachlorocyclohexane (BHC) as a model histopathological, histoenzymological, biochemical, and electrophoretic studies were undertaken to find out certain parameters for early diagnosis of liver cancer. In addition, cytogenetic studies were carried out to evaluate the effect of BHC feeding on mitotic and meiotic divisions. The results of these investigations suggest that there is a significant change in liver weight in experimental group. Histologically, liver cells follow a definite sequential cellular alteration ultimately leading to liver tumor. Histochemically, well defined pattern of glycogen accumulation and iron distribution in hepatocytes was observed. The electron-microscopic observation demonstrated prominently the proliferation of agranular endoplasmic reticulum in early stages. The distribution of certain enzymes linked with plasma membrane, lysosomes, and mitochondria showed the functional alteration of these organelles both in neoplastic nodules and tumours induced by BHC. The biochemical changes observed in gluconeogenic enzymes (G6Pase and F1,6dipase) and dehydrogenases (LDH, ICDH, and MDH) at different duration of exposure to BHC indicated decrease in enzyme activity of both gluconeogenic pathway and tricarboxylic acid cycle, linked with energy metabolism. These changes tend to recover with discontinuation of BHC but 8 months continuous feeding produces irreversible changes in G6Pase activity. Using polyacrylamide gel electrophoresis technique a change in serum proteins and LDH isoenzymes was observed. However, extrapolation of these findings to human situation needs more extensive studies, taking into account all possible variables, such as the DDT and BHC load in our environment and the body burden resulting there from.

Polybrominated biphenyl toxicosis in the rat and mouse

Rats and mice were given 22 oral doses of Firemaster FF-1 or pure 2,2′,4,4′,5,5′-hexabromobiphenyl (HBB) over a 30-day period and held for 90 additional days to determine the pathobiological manifestations of toxicity. Female mice and rats given Firemaster FF-1 became porphyric after 45 and 120 days, respectively. The liver was enlarged due to swelling of hepatocytes, fatty infiltration and proliferation of endoplasmic reticulum. There was a marked increase in serum protein which was primarily due to β-globulin fraction in the rat. γ-Glutamyl transpeptidase was elevated in female rats in both groups given Firemaster FF-1 and HBB. A significant dose related increase in serum glutamic pyruvic transaminase was found in male rats at Day 60 only. There was a decrease in the packed cell volume accompanied by a proportional decrease in hemoglobin and red blood cell values in male rats given 30 mg of FF-1 at 30 and 45 days but returned to normal at 60 and 90 days. Hepatocellular alterations in rats and mice given FF-1 at 30.0 mg/kg (22 total doses) persisted when examined at 120 days. FF-1 was more toxic than pure HBB as determined by measurement of porphyrins and pathologic findings. Rats or mice treated with HBB tended to recover when examined during postexposure periods.

Ultrastructural alterations in the liver of rats fed photomirex (8-Monohydromirex)

Alterations in the liver of rats fed photomirex or mirex for 28 d have been studied by electron microscopy. A dose of 0.05 or 0.5 ppm photomirex produced selective ultrastructural damage to the mitochondria of hepatocytes. The parenchymal cells had a proliferation of smooth-surfaced endoplasmic reticulum (SER) with a concomitant depletion of glycogen, a reduction of rough-surfaced endoplasmic reticulum (RER) profiles, an abnormal accumulation of lipid droplets, and pleomorphic nuclei at the 5 ppm photomirex level. In the animals receiving 50 ppm photomirex there were degenerating foci in the organ. There was an increase of electron-dense bodies in the hepatocytes from the 5 ppm mirex group but these cells, in the animals receiving 50 ppm mirex, had SER proliferation and glycogen depletion. It is concluded that photomirex causes more severe ultrastructural changes in the livers of rats than mirex.

Effects of human chorionic gonadotropins on the interstitial cells of the rat testis: A morphometric and radioimmunological study.

The effects of human chorionic gonadotropins (hCG) on the rat testicular interstitial cells (Leydig cells) were investigated by stereologic and radio-immunological methods. Short-term (2 h's) hCG-administration induced only lipid depletion in the Leydig cells. Chronic hCG-treatment provoked a significant cell hypertrophy, which was mainly due to smooth endoplasmic reticulum proliferation; the surface area of mitochondrial cristae, and the volume of the lipid and peroxisome compartments were also significantly increased. These morphologic findings are discussed in the light of radioimmunological data, showing that chronic hCG-administration increased the steroidogenic capacity (testosterone output) of the Leydig cells.

Ultrastructural studies on the vitamin D induced heart lesions in the rat

Ultrastructure of the heart in rats treated with high doses of vitamin D was investigated. On the fourth day after 280 000 to 300 000 iu of either vitamin D 2 or D 3 administration in three or four intraoral doses, a massive heart lesion was observed. Various forms of cardiac necrosis were seen, as well as calcium deposits within otherwise unaltered cardiac cells. Independently of the necrotic myocytes and of the changes in coronary blood vessels, focal stimulation of both cardiomyocytes and of interstitial cells was found with a vivid proliferation of endoplasmic reticulum, a decrease in the amount of myofibrils as well as the appearance of myelin-like structures and calcium deposits. A complex pathogenesis of the heart lesion caused by vitamin D treatment is suggested. The main pathogenic factors seem to be a massive calcium transport into the cell and its consequences, cardiotoxic and coronarogenic necrosis, although the ultrastructure of the hearts seems to point also to some other mechanisms of the cardiomyopathy observed in the rats treated with high doses of vitamin D.

In vivo administration of hydroxylated phenobarbital metabolites: effect on rat hepatic cytochromes P-450, epoxide hydrolase and udp-glucuronosyltransferase

p-Hydroxyphenobarbital and m-hydroxyphenobarbital injected intraperitoneally to rats at the dose of 80 mg/kg induced a small increase of cytochrome P-450 in crude liver homogenate (expressed as nmoles/g liver) but a decrease of cytochrome P-450 concentration in isolated microsomes (expressed as nmoles/mg microsomal protein). A similar decrease of NADPH-cyt c reductase and epoxide hydrolase specific activities was observed. Pretreatment of animals with phenobarbital metabolites did not alter the native UDP-glucuronosyltransferase, but depressed the specific activity of digitonin-treated UDP-glucuronosyltransferase towards p-nitrophenol. Gel electrophoresis of microsomes showed that p-hydroxyphenobarbital and m-hydroxyphenobarbital did not induce a net biosynthesis of proteins with molecular weight near 50,000. Qualitative examination of monooxygenase activities indicated that the administration of hydroxylated phenobarbital did not modify the catalytic characteristics of microsomes, as compared with those of control microsomes. When phenobarbital and its p-hydroxyderivative were simultaneously injected to rats, specific enzyme activities of microsomes were increased as compared with controls but remained lower than with phenobarbital alone. The qualitative characteristics of the monooxygenase system were similar to those of microsomes from phenobarbital-induced rats. It may be concluded that phenobarbital produces both a proliferation of endoplasmic reticulum and an induction of drug-metabolizing activities, whereas its hydroxylated metabolites only retain the prolifer-ative activity: thus, these two effects of phenobarbital might depend on two different molecular mechanisms.

Juvenile hormone-stimulated proliferation of endoplasmic reticulum in fat body cells of a vitellogenic insect, [formula omitted] (Blattaria)

The rate of incorporation of [ 14C]choline or [ 32P]orthophosphate into phospholipids of rough and smooth-surfaced microsomal membranes from insect fat body was stimulated by juvenile hormone. The maximum incorporation rate in vivo occurred three days following hormone application. During in vitro incubation of the fat bodies from hormone-treated females [ 32P] was taken up by the cells at about twice the rate of the controls, but its incorporation into microsomes was elevated 3.5 to five-fold. No difference in [ 32P] precursor pools was observed in vivo . The enhanced proliferation of endoplasmic reticulum is temporally coupled to the hormone-induced de novo biosynthesis of an exportable protein, vitellogenin.

Serum bile acid concentration in some experimental liver lesions of rat

The usefulness of measuring serum bile acid concentrations by RIA in a number of acute experimental liver injuries of rats was assessed by comparing the concentrations with the results of some of the routinely employed methods of examining hepatotoxic changes. Centribular liver cell injury produced by CCl 4 revealed leakage of GPT and GDH and to a lesser extent AP; along with minimal increase in serum bile acid levels. Serum bilirubin concentration remained unchanged. Surgical bile duct ligation resulted in marked rises in AP, GPT and GDH and total bilirubin levels and levels of serum bile acids. Intravenous injection of MnSO 4 induced focal necrosis of liver and bile canalicular dilation associated with elevated GDH and GPT concentrations. AP and bilirubin levels were unchanged. Bile acid levels were raised among female rats. 2,4-Xylidine induced hepatotoxicity revealed bile duct hyperplasia, liver cell enlargement, liver cell necrosis, biliary canalicular dilation and proliferation of endoplasmic reticulum. GDH and GPT levels were raised along with bile acid concentrations. This study suggested that assay of bile acid concentration is a sensitive indicator of several acute hepatic injuries.

Ultrastructural and Enzymic Studies of Cell Membranes from Ice-encased and Noniced Winter Wheat Seedlings

A marked increase in the amount of cisternal-like cytoplasmic membranes was observed after ice encasement of winter wheat (Triticum aestivum L.) seedlings. Linear sucrose gradients were employed to separate the various membrane components of the microsomal membrane fraction. NADH- and NADPH-cytochrome c reductase, two specific enzyme markers for plant endoplasmic reticulum (ER) were used to locate the ER in the linear gradients. The identity of the ER fraction was confirmed by determining the effect of EDTA and Mg(2+) in the preparative media on the distribution of NADH- and NADPH-cytochrome c reductase activity within the gradient. In the presence of EDTA which dissociates ribosomes from ER, peaks of activity for the two enzymes were observed at a density corresponding to that for "smooth" ER. When the media also contained an appropriate concentration of Mg(2+) to maintain the attachment of ribosomes to the ER, the peaks of activity for the enzymes shifted to a density corresponding to that for "rough" ER. NADH-cytochrome c reductase activity was similar for 24 C-grown and 2 C-grown iced seedlings, but significantly lower for 2 C noniced seedlings. No preferential increase in uptake of radioactive leucine or choline in the ER was observed during ice encasement. The accumulation of electron microscopically visible membrane arrays was not inhibited by the presence of protein synthesis inhibitors at concentrations which severely inhibited incorporation of [1-(14)C]leucine into membrane protein, but did not affect survival and growth of the seedlings. These observations indicate that the apparent proliferation of ER during ice encasement does not result from net membrane synthesis, but rather from reorganization of existing membrane elements within the cell.

Metabolic and Ultrastructural Changes Associated with Flooding at Low Temperature in Winter Wheat and Barley

Cold-hardened winter wheat (Triticum aestivum L. cv. Fredrick) and winter barley (Hordeum vulgare L. cv. Dover) were exposed to total flooding at 2 C. Dover seedlings were damaged more quickly than Fredrick, and after 3 weeks of flooding the survival of Dover was reduced to 10% and Fredrick to about 50%. Tissue moisture was slightly greater in Dover than Fredrick throughout the 4-week flooding period. Carbon dioxide and ethanol accumulated throughout the 4-week flooding period in both cultivars. Lactic acid increased rapidly during the 1st week of flooding, and remained relatively constant during the remainder of the flooding period. Oxygen consumption of seedling shoot tissue after exposure to flooding declined abruptly after only 1 day of flooding, but recovered somewhat during the subsequent 2 weeks. The effect of flooding was more pronounced on the ultrastructure of Dover than Fredrick. Although proliferation of endoplasmic reticulum was observed in the early stages of flooding in both cultivars, the occurrence of distinct parallel arrays and concentric whorls of membranes was prevalent in the flooded barley. Severe ultrastructural damage to a large proportion of apical cells in both cultivars was observed after 2 to 3 weeks of flooding.

Ultrastructure of spontaneous liver lesions in cynomolgus and rhesus monkeys

During routine ultrastructural examination of livers from rhesus and cynomolgus monkeys, a variety of spontaneous lesions was encountered. The changes included: foci of inflammatory cells, necrotic foci, fatty change, paracrystalline mitochondrial inclusions, cytoplasmic clefts, myelinoid bodies and smooth endoplasmic reticulum proliferation. The ultrastructural appearance of these findings is described and their possible significance discussed.

Ultrastructural effects of formulated picloram on leaflets of velvet mesquite and catclaw acacia*

Summary:The effects of picloram formulated with a nonionic surfactant (X‐77) and of the surfactant alone on the ultrastructure of leaf cells of velvet mesquite (Prosopis velutina Woot.) and catclaw [Acacia greggii var. ariznica (Gray) Isely] were examined The surfactant induced temporary protrusions from chloroplasts in both species. A proliferation of rough endoplasmic reticulum (RER) was noted in velvet mesquite within 8h of application of the herbicide and in catclaw with in 27 h. By 72h after treatment. both species exhibited distortions of organelles with more severe symptoms in catclaw. the species more sensitive to the herbicide Leaf abscission occurred subsequently and was more pronounced in catclaw than in mesquitel It is known that RER proliferation is induced by ethylene and that ethylene evolution is stimulated by picloram. The present study suggests that the interaction between these two chemicals was similar in the two plant species studied.

Effects of Glucocorticoids on Microsomal Membrane Synthesis in Hepatocytes from Adrenalectomized Rats*

Biochemical and morphological studies were performed on livers from normal, adrenalectomized (ADX), and ADX and dexamethasone (DEX)-treated rats to investigate the effects of glucocorticoids on microsomal membrane synthesis. Overnight fasted normal, ADX and ADX rats treated 2 or 4 h with DEX received [3H]leucine and [14C]glycerol. Livers were removed, and tissue specimens were prepared for electron microscopy and tissue fractionation. Liver microsomal subfractions were prepared and subsequently washed to produce rough and smooth microsomal membranes. Radioactivity and membrane composition were determined, and glucose-6-phosphatase activity was measured in washed microsomal membranes. Adrenalectomy caused decreased microsomal membrane synthesis. Two and 4 h of DEX administration restored microsomal membrane synthesis to normal levels. ADX also caused an alteration in composition of the microsomal membranes (reflected in decreased phospholipid-protein ratios), which was restored to normal levels by 4 h after DEX administration. The earliest effects of the hormone on membrane synthesis were observed in smooth microsomes as part of a smooth endoplasmic reticulum (SER) proliferation. These findings were supported by observations made with the electron microscope. The proliferating SER was enriched in at least one component: glucose-6-phosphatase. Although the specific relationship of SER to glucocorticoid action remains unclear, the interpretation is offered that SER proliferation and alteration in glucose-6-phosphatase distribution are component parts of the total response of the hepatocyte to glucocorticoids.