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At least 343 records · Page 19Linked to original sources
PubMed1996

Sarcoplasmic reticulum calcium uptake in human myocardium subjected to ischemia and reperfusion during cardiac surgery.

We evaluated the effect of ischemia and reperfusion on sarcoplasmic reticulum Ca uptake in patients subjected to cardiac surgery. Our series included 16 patients (seven female, nine male, age 63 +/- 2 years): five were subjected to aortic valve replacement, five to aortic and mitral valve replacement, six to coronary artery bypass graft. In each case no clinical, electrocardiographic or echocardiographic evidence of perioperative infarction was observed. Biopsies were obtained from the right atrium of each patient before starting extracorporeal circulation, and after the recovery of spontaneous contractile activity, i.e. after cardioplegia-ischemia-reperfusion. The tissue was homogenized, and oxalate-supported Ca uptake, which represents sarcoplasmic reticulum Ca uptake, was measured in the unfractionated homogenate. The assay was performed under basal conditions and in the presence of 900 microM ryanodine, in order to block sarcoplasmic reticulum Ca release channels. Under basal conditions at pCa = 5.85 the rate of sarcoplasmic reticulum Ca uptake averaged 4.76 +/- 0.37 nmol/min per mg of protein in the pre-ischemic samples, and decreased significantly in the post-ischemic samples (3.09 +/- 0.29 nmol/min per mg, P < 0.01). A significant decrease of Ca uptake after ischemia and reperfusion was observed also in the presence of ryanodine (3.53 +/- 0.48 nmol/min per mg) compared to pre-ischemic values (5.98 +/- 0.56 nmol/min per mg, P < 0.01). Additional experiments showed no change in the Ca sensitivity of Ca uptake in the postischemic samples (Kca = 0.48 +/- 0.02 microM, no significant difference after ischemia and reperfusion). In conclusion, active sarcoplasmic reticulum Ca transport was impaired in human atrial myocardium after reversible ischemia and reperfusion.

Aged↗
PubMed1988

Lysophospholipid-mediated alterations in the calcium transport systems of skeletal and cardiac muscle sarcoplasmic reticulum.

The effects of various lysophospholipids on the calcium transport activity of sarcoplasmic reticulum (SR) from rabbit skeletal and canine cardiac muscles were examined. The lipids decreased calcium transport activity in both membrane types; the effectiveness being in the order lysoPC greater than lsyoPS, lysoPG greater than lysoPE. The maximum inhibition induced by lysoPC, lysoPG and lysoPS was greater than 85% of the normal Ca2+-transport rate. In cardiac SR lysoPE had a maximal inhibition of about 50%. Half maximal inhibition of calcium transport by lysoPC was achieved at 110 nmoles lysoPC/mg SR. At this concentration of lysoPC, the (Ca2+ + Mg2+)-ATPase and Ca2+-uptake activities were inhibited to the same extent (about 60%) in skeletal sarcoplasmic reticulum, while in cardiac sarcoplasmic reticulum, there was less than 20% inhibition of the Ca2+ + Mg2+-ATPase activity. Studies with EGTA-induced passive calcium efflux showed that up to 200 nmoles lysoPC/mg SR did not alter calcium permeability significantly in cardiac sarcoplasmic reticulum. In skeletal muscle membranes the lysophospholipid mediated decrease in calcium uptake correlated well with the increase in passive calcium efflux due to lysophosphatidylcholine. The difference in the lysophospholipid-induced effects on the sarcoplasmic reticulum from the two muscle types probably reflects variations in protein and other membrane components related to the respective calcium transport systems.

Adenosine Triphosphatases↗
PubMed1994

Involvement of the sarcoplasmic reticulum calcium pump in myocardial contractile dysfunction: comparison between chronic pressure-overload and stunning.

Acute as well as chronic forms of heart failure involve mechanical dysfunction during systole and/or diastole. The rapid Ca2+ release from and Ca2+ reuptake into the tubuli of the sarcoplasmic reticulum are processes that critically determine normal systolic and diastolic myocardial function, which explains why in the last fifteen years so much attention has been paid to understand the performance of the sarcoplasmic reticulum Ca2+ pump during myocardial contractile dysfunction. In this communication we have reviewed the literature data on sarcoplasmic reticulum Ca2+ pump function in the chronically pressure-overloaded hypertrophied and stunned (post-ischemic reversibly injured) myocardium in the light of some new data from our laboratory. Results on the pressure-overloaded hypertrophied myocardium provide evidence that impaired relaxation is most likely due to a low capacity of the sarcoplasmic reticulum to pump Ca2+, a consequence of a lower density of Ca(2+)-pumping sites within the sarcotubular membranes. Contractile dysfunction in stunned myocardium is accompanied by an upregulation of the sarcoplasmic reticulum Ca2+ ATPase gene resulting in a slight increase of the Ca2+ pumping activity. The latter increase is likely an adaptive response of the reversibly injured myocardium which may contribute to the slow recovery of contractile function.

Calcium-Transporting ATPases↗
PubMed1993

The endoplasmic reticulum-associated VP7 of rotavirus is targeted to axons and dendrites in polarized neurons.

Rotavirus, which matures and is retained in the endoplasmic reticulum, was used to examine how polarized dorsal root ganglion and spinal cord neurons distributed cytoplasmic and endoplasmic reticulum-associated proteins. A remarkable observation was that NS28, a trans-endoplasmic reticulum-membrane protein which functions as a receptor for budding particles, remained in the cell body during the whole course of infection (48 h) while the VP7 glycoprotein, which is endoplasmic reticulum associated and usually retained in the endoplasmic reticulum, was targeted to axons already 4 h post infection. VP7 was furthermore transported in an endo-beta-N-acetylglucosaminidase H sensitive form through the secretory pathway. The segregated appearances of NS28 and the endo-beta-N-acetylglucosaminidase H sensitive VP7 indicate that VP7 enters a transport compartment separate from NS28. Brefeldin A treatment rapidly disintegrated the Golgi apparatus of the neurons and rapidly blocked axonal transport of Sendai virus glycoproteins, while axonal transport of rotavirus VP7 was not blocked, suggesting that VP7 uses an intracellular pathway in neurons which does not involve the Golgi apparatus.

Animals↗
PubMed1986

Freeze-fractured sarcoplasmic reticulum in adult and embryonic fast and slow muscles.

There is evidence to suggest that 8 nm calcium transport particles in the sarcoplasmic reticulum are involved in the regulation of twitch properties in adult muscles. We have studied ultrastructural characteristics of the sarcoplasmic reticulum in relation to previously defined physiological changes that take place in the normal course of development. The fast twitch posterior latissimus dorsi (PLD) and the slow tonic anterior latissimus dorsi (ALD) of the chicken were compared using the procedure of freeze-fracture. In the adult PLD, the sarcoplasmic reticulum was composed of longitudinal tubules which gave rise to fenestrated cisternae at the centre of the H band and to terminal cisternae that form triads regularly at each A-I junction. In most of the fibres (85%), 8 nm intramembrane particles were closely packed in the concave fracture face (P-face). In the ALD, a tubular network with an open circular pattern extended the entire length of the A band and usually throughout the I band as well. Dyads or triads, which were infrequent, were often oriented obliquely. The density of intramembrane particles was low in the majority of the fibres, but there was a significant minority population (30%) in which particle density was relatively high. At 10 days in ovo, when speed of contraction in both the ALD and PLD is slow, there was a circular configuration of sarcoplasmic reticulum components in both muscles, and particle density was low. Surprisingly, at 18 days in ovo, when the rate of tension development and relaxation have reached nearly adult values in the fast PLD, this muscle, like the ALD, continued to exhibit a circular arrangement of sarcoplasmic reticulum tubules. The density of P-face particles, although greater than at 10 days, was still low relative to the adult PLD. Estimated values for the 18-day PLD were similar to those calculated for the adult slow muscle. Our observations, along with those of other investigators, suggest that abundant intramembrane particles may be related to the fast twitch properties of the adult PLD. However, they indicate that neither the pattern of membranes typical of the adult fast muscle nor the high content of calcium transport particles is required for the differentiation of fast twitch characteristics.

Animals↗
PubMed1980

Functional heterogeneity of the sarcoplasmic reticulum within sarcomeres of skinned muscle fibers.

Precipitation of Ca oxalate in the sarcoplasmic reticulum of chemically skinned rabbit psoas fibers caused an increase in light scattering which was proportional to the amount of Ca accumulated per unit fiber volume. The increase in scattering was used to measure net accumulation rates and steady-state Ca capacities of the sarcoplasmic reticulum in single fibers. The data obtained were qualitatively and quantitatively similar to those reported for isolated vesicle preparations. Under conditions in which Ca was not depleted from the medium, Ca accumulation was linear with time over much of its course. Steady-state capacities were independent of the Ca concentration; uptake rates were half-maximal at 0.5 microM Ca++ and saturated above about 1.0 microM. Both rate and capacity varied with the oxalate concentration, being maximal at oxalate concentrations greater than or equal to mM and decreasing in proportion to one another at lower concentrations, with a threshold near 0.25 mM. At the lower loads, electron micrographs showed many sarcoplasmic reticulum elements empty of precipitate alongside others that were full, whereas virtually all were filled in maximally loaded fibers. These data indicate that the Ca oxalate capacity of each fiber varies with the number and volume of elements in which Ca oxalate crystals can form at a given oxalate concentration, and that individual regions of the sarcoplasmic reticulum within each sarcomere differ in their ability to support Ca oxalate precipitation. Our working hypothesis is that this range in ability to form Ca oxalate crystals involves differences in ability to accumulate and retain ionized Ca inside the sarcoplasmic reticulum.

Adenosine Triphosphate↗
PubMed1978

Evidence for a K+, Na+ permeable channel in sarcoplasmic reticulum.

Potassium and sodium cation permeabilities of skeletal sarcoplasmic reticulum vesicles were characterized by means of 3H-choline, 22Na+ and 86Rb+ isotope efflux and membrane potential measurements. Membrane potentials were generated by diluting K gluconate filled sarcoplasmic reticulum vesicles and liposomes into Tris or Na gluconate media, in the presence or absence of valinomycin, and were measured using the voltage-sensitive membrane probe 3,3'-dipentyl-2,2'-oxacarbocyanine. About 2/3 of the sarcoplasmic reticulum vesicles, designated Type I, were found to be permeable to Rb+, K+ and Na+. The remaining 1/3, Type II vesicles, were essentially impermeable to these ions. The two types of vesicles were impermeable to larger cations such as choline or Tris. Both were present in about the same ratio in fractions derived from different parts of the reticulum structure. Studies with cations of different size and shape suggested that in Type I vesicles permeation was restricted to molecules fitting through a pore with a cross-section of 4--5 A by 6 A or more. When vesicles were sonicated, vesicles permeable to K+ decreased more than those impermeable to K+. These data suggest the existence of K+, Na+ permeable channels which are probably randomly dispersed in the intact reticulum structure at an estimated density of 50 pores/micrometer2. The function of the channel may be to allow rapid K+ movement to counter Ca2+ fluxes during muscle contraction and relaxation.

Animals↗
PubMed1983

Osmotic changes of sarcoplasmic reticulum vesicles during Ca2+ uptake.

The ATP-dependent accumulation of Ca2+ by sarcoplasmic reticulum vesicles at 37 degrees reaches a peak after approximately 100 sec. The Ca2+-loading level then declines until a steady-state level is reached which is 20% less than the peak value. This spontaneous release of Ca2+ is enhanced by inclusion of maleate in the Ca2+ uptake medium. Increasing the extravesicular osmolarity by the addition of sucrose to the Ca2+ uptake medium prevents spontaneous Ca2+ release and increases the steady-state Ca2+-loading capacity of sarcoplasmic reticulum vesicles. Swelling of sarcoplasmic reticulum vesicles during Ca2+ uptake in medium containing sucrose is indicated by changes in the light-scattering intensity. These experiments indicate that the capacity of sarcoplasmic reticulum vesicles to accumulate Ca2+ is limited by the osmotic gradient generated by the increase in intravesicular Ca2+. Swelling of sarcoplasmic reticulum vesicles during Ca2+ uptake causes spontaneous Ca2+ release.

Animals↗
PubMed1979

Stereological study of endoplasmic reticulum, Golgi complex and secretory granules in the B-cells of normal and alloxan-treated mice.

Different B-cell organelles (lamellar and vesicular endoplasmic reticulum, Golgi complex, whole secretory granules and secretory granule cores) were studied stereologically in pancreatic islets from control mice and mice killed 10 or 60 min following alloxan injection. Ten min following alloxan a significant decrease was observed in the volume, surface and numerical densities of whole secretory granules and their cores, and a significant increase was found in the volume and surface densities of vesicular endoplasmic reticulum. At the 60 min observation time, a significant decrease was seen in the volume density of lamellar endoplasmic reticulum and Golgi complex, and in the volume, surface and numerical densities of whole secretory granules and their cores, and a significant increase was observed in the volume and surface densities of vesicular endoplasmic reticulum, and in the mean values for volume and surface of whole secretory granules and their cores. The stereological data indicate swelling of endoplasmic reticulum, decreased Golgi area, and decreased number and total volume and surface of secretory granules during the first hour after alloxan administration to mice. The observations may be consistent with inhibited insulin synthesis.

Alloxan↗
PubMed2005

Mice conditionally lacking the Wolfram gene in pancreatic islet beta cells exhibit diabetes as a result of enhanced endoplasmic reticulum stress and apoptosis.

AIMS/HYPOTHESIS: Wolfram syndrome is an autosomal recessive disorder characterised by childhood diabetes mellitus, optic atrophy and severe neurodegeneration, resulting in premature death. The aim of this study was to investigate the mechanisms responsible for the phenotype of carbohydrate intolerance and loss of pancreatic beta cells in this disorder. MATERIALS AND METHODS: To study the role of the Wolfram gene (Wfs1) in beta cells, we developed a mouse model with conditional deletion of Wfs1 in beta cells by crossing floxed Wfs1 exon 8 animals with mice expressing Cre recombinase under the control of a rat insulin promoter (RIP2-Cre). Complementary experiments using RNA interference of Wfs1 expression were performed in mouse insulinoma (MIN6) cell lines (WfsKD). RESULTS: Male knockout mice (betaWfs(-/-)) began developing variable and progressive glucose intolerance and concomitant insulin deficiency, compared with littermate controls, by 12 weeks of age. Analysis of islets from betaWfs(-/-) mice revealed a reduction in beta cell mass, enhanced apoptosis, elevation of a marker of endoplasmic reticulum stress (immunoglobulin heavy chain-binding protein [BiP]), and dilated endoplasmic reticulum with decreased secretory granules by electron microscopy. WfsKD cell lines had significantly increased apoptosis and elevated expression of the genes encoding BiP and C/EBP-homologous protein (CHOP), two markers of endoplasmic reticulum stress. CONCLUSIONS/INTERPRETATION: These results indicate that (1) lack of expression of Wfs1 in beta cells was sufficient to result in the diabetes mellitus phenotype; (2) beta cell death occurred by an accelerated process of apoptosis; and (3) lack of Wfs1 was associated with dilated endoplasmic reticulum and increased markers of endoplasmic reticulum stress, which appears to be a significant contributor to the reduction in beta cell survival.

Animals↗
PubMed2003

Ultrastructural analysis of transitional endoplasmic reticulum and pre-Golgi intermediates: a highway for cars and trucks.

Cargo selection and export from the endoplasmic reticulum occurs at specialized sites in cells. Export complexes consist of transitional elements of the endoplasmic reticulum and pre-Golgi intermediates. It is generally assumed that 60 to 80 nm initially COPII-coated vesicles derived from the transitional endoplasmic reticulum are the main carriers for transport of cargo to the Golgi apparatus. We have analyzed on serial ultrathin sections the transitional endoplasmic reticulum and pre-Golgi intermediates of beta cells of islets of Langerhans in mouse pancreas. In addition to Golgi-associated complexes, others were observed in the periphery of the cells or close to the nuclear envelope. Upon three-dimensional reconstruction, non-coated ribosome-free tubules with an average diameter of 115 nm (range 60-195 nm) and a length of up to 500 nm were detected in the pre-Golgi intermediates in addition to small vesiculo-tubular elements. Furthermore, evidence was found that the large tubular elements may directly arise from transitional elements of the endoplasmic reticulum. In a given cell, pre-Golgi intermediates were found to be composed solely of small vesiculo-tubular elements or additionally of tubules or solely of tubules. Immunogold labeling for proinsulin indicated that the large tubular elements contained cargo and thus appear to take part in ER-to-Golgi transport.

Animals↗
PubMed2002

Sarcoplasmic reticulum function in slow- and fast-twitch skeletal muscles from mdx mice.

The aim of the present study was to establish whether alterations in sarcoplasmic reticulum function are involved in the abnormal Ca(2+) homeostasis of skeletal muscle in mice with muscular dystrophy ( mdx). The properties of the sarcoplasmic reticulum and contractile proteins of fast- and slow-twitch muscles were therefore investigated in chemically skinned fibres isolated from the extensor digitorum longus (EDL) and soleus muscles of normal (C57BL/10) and mdx mice at 4 and 11 weeks of development. Sarcoplasmic reticulum Ca(2+) uptake, estimated by the Ca(2+) release following exposure to caffeine, was significantly slower in mdx mice, while the maximal Ca(2+) quantity did not differ in either type of skeletal muscle at either stage of development. In 4-week-old mice spontaneous sarcoplasmic reticulum Ca(2+) leakage was observed in EDL and soleus fibres and this was more pronounced in mdx mice. In addition, the maximal Ca(2+)-activated tension was smaller in mdx than in normal fibres, while the Ca(2+) sensitivity of the contractile apparatus was not significantly different. These results indicate that mdx hindlimb muscles are affected differently by the disease process and suggest that a reduced ability of the Ca(2+)-ATPase to load Ca(2+) and a leaky sarcoplasmic reticulum membrane may be involved in the altered intracellular Ca(2+) homeostasis.

Animals↗
PubMed1997

The effects of changes to action potential duration on the calcium content of the sarcoplasmic reticulum in isolated guinea-pig ventricular myocytes.

We have estimated sarcoplasmic reticulum calcium content using rapid application of caffeine on voltage clamped, isolated guinea-pig ventricular myocytes. Caffeine induces the release of calcium from the sarcoplasmic reticulum and this calcium is extruded from the cells by the sarcolemmal Na/Ca exchange. Integrating the inward Na/Ca exchange current thus allows estimations of sarcoplasmic reticulum calcium content. Ventricular myocytes were stimulated to reach new steady-states by action potential voltage clamps of varying duration. Once contractile steady-state had been reached caffeine was rapidly applied in place of the next action potential and sarcoplasmic reticulum calcium content measured. Prolonging the action potential duration increased sarcoplasmic reticulum calcium content and vice-versa. This calcium loading may underlie the positive inotropic effect of increased action potential duration.

Action Potentials↗
PubMed1996

Maleate modifies apical endocytosis and permeability of endoplasmic reticulum membranes in kidney tubular cells.

Previous studies have shown that histochemical modifications of the endoplasmic reticulum in epithelial cells might be related to their transport function. We have examined the effect of sodium maleate, which produces generalized transport derangement reminiscent of Fanconi syndrome, on the organization, morphology and enzyme activities of endoplasmic reticulum in rat kidney cells. The osmium impregnation technique has revealed that apical vacuoles increase in volume and in number in most proximal tubule cells, and contain osmium deposits. Osmium impregnation of the endoplasmic reticulum is much reduced. In vitro studies, performed with isolated microsomes, show NADPH cytochrome c reductase activity in both normal and maleate-treated rats. As revealed by vanadate, Ca+-ATPase activity in isolated microsomes is unnaffected by maleate but the vanadate-insensitive or passive component of calcium uptake increases particularly later in the response. Therefore, the remaining calcium uptake in the presence of vanadate is indeed passive; in vivo maleate administration also appears to increase the passive entry of calcium into the microsomal compartment. The morphological and histochemical alterations of the endoplasmic reticulum cisternae occur rapidly and with a similar time course to the transport defects, suggesting that this organelle plays a role in transcellular transport. Maleate may directly affect the endoplasmic reticulum membranes whereby passive permeability to calcium is increased. The endocytotic apparatus and possibly exocytosis phenomena are modified by maleate as shown by the increased vacuolization and the presence of black osmium deposits in vacuoles.

Animals↗
PubMed1991

Effect of brief regional ischemia followed by reperfusion with or without superoxide dismutase and catalase administration on myocardial sarcoplasmic reticulum and contractile function.

The effect of reperfusion with and without free radical scavengers on sarcoplasmic reticulum and contractile function was examined in a canine model of 15-minute coronary artery occlusion followed by reperfusion. Dogs were reperfused with (n = 13) or without (n = 16) superoxide dismutase and catalase or were killed at 15 minutes of ischemia (n = 17). Superoxide dismutase and catalase were administered as a bolus (20,000 and 12,500 U/kg, respectively) beginning 1.25 minutes before reperfusion followed by infusion of 16,000 and 12,500 U/kg/hr, respectively. Sarcoplasmic reticulum function was evaluated from the rate of calcium uptake of unfractionated subepicardial, subendocardial, and transmural homogenates determined with and without ruthenium red to close the calcium release channel. Mechanical function was evaluated by means of sonomicrometry. Fifteen minutes of ischemia significantly (p less than 0.05) depressed the sarcoplasmic reticulum calcium uptake rate only in the subendocardium (from 25 +/- 2 to 14 +/- 1 nmol/min/mg without ruthenium red and from 60 +/- 3 to 49 +/- 3 nmol/min/mg with ruthenium red). Reperfusion with or without superoxide dismutase and catalase restored homogenate calcium uptake rates to normal, although severe contractile dysfunction persisted. This indicates that damage to the sarcoplasmic reticulum may not be the major cause of postreperfusion contractile dysfunction. Ischemia-reperfusion caused a decrease in systolic shortening from 19 +/- 2% to 1 +/- 2% with and from 18 +/- 1% to 4 +/- 1% without free radical scavengers (p = NS between groups). Thus administration of superoxide dismutase and catalase beginning shortly before reperfusion had no effect on postreperfusion contractile dysfunction or sarcoplasmic reticulum function.

Animals↗
PubMed1988

Oxygen radical-mediated lipid peroxidation and inhibition of Ca2+-ATPase activity of cardiac sarcoplasmic reticulum.

Oxygen radicals have been implicated as important mediators of myocardial ischemic and reperfusion injury. A major product of oxygen radical formation is the highly reactive hydroxyl radical via a biological Fenton reaction. The sarcoplasmic reticulum is one of the major target organelles injured by this process. Using a oxygen radical generating system consisting of dihydroxyfumarate and Fe3+-ADP, we studied lipid peroxidation and Ca2+-ATPase of cardiac sarcoplasmic reticulum. Incubation of sarcoplasmic reticulum with dihydroxyfumarate plus Fe3+-ADP significantly inhibited enzyme activity. Addition of superoxide dismutase, superoxide dismutase plus catalase (15 micrograms/ml) or iron chelator, deferoxamine (1.25-1000 microM) protected Ca2+-ATPase activity. Time course studies showed that this system inhibited enzyme activity in 7.5 to 10 min. Similar exposure of sarcoplasmic reticulum to dihydroxyfumarate plus Fe3+-ADP stimulated malondialdehyde formation. This effect was inhibited by superoxide dismutase, catalase, singlet oxygen, and hydroxyl radical scavengers. EPR spin-trapping with 5,5-dimethyl-1-pyrroline-N-oxide verified production of the hydroxyl radical. The combination of dihydroxyfumarate and Fe3+-ADP resulted in a spectrum of hydroxyl radical spin trap adduct, which was abolished by ethanol, catalase, mannitol, and superoxide dismutase. The results demonstrate the role of oxygen radicals in causing inactivation of Ca2+-ATPase and inhibition of lipid peroxidation of the sarcoplasmic reticulum which could possibly be one of the important mechanisms of oxygen radical-mediated myocardial injury.

Adenosine Diphosphate↗
PubMed1988

Characterization of membrane-bound electron transport enzymes from castor bean glyoxysomes and endoplasmic reticulum.

Membranes purified from castor bean endosperm glyoxysomes by washing with sodium carbonate exhibited integral NADH:ferricyanide and NADH:cytochrome c reductase activities. The enzyme activities could not be attributed to contamination by other endomembranes. Purified endoplasmic reticulum membranes also contained the redox activities; and marker enzyme analysis indicated minimum cross contamination between glyoxysomal and endoplasmic reticulum fractions. The glyoxysomal redox activities were optimally solubilized at detergent to protein ratios (weight to weight) of 10 (Triton X-100), 50 (3-[3-cholamidopropyl)-dimethylammonio]-1-propanesulfonate), and 100 (octylglucoside). Detergent in excess of the solubilization optimum was stimulatory to NADH:ferricyanide reductase and inhibitory to NADH:cytochrome c reductase. Endoplasmic reticulum redox activity solubilization profiles were similar to those obtained for glyoxysomal enzymes using Triton X-100. Purification of the glyoxysomal and endoplasmic reticulum NADH:ferricyanide reductases was accomplished using dye-ligand affinity chromatography on Cibacron blue 3GA agarose. Sodium dodecyl sulfate-polyacrylamide gel electrophoretic analysis of NADH:ferricyanide reductase preparations purified by rate-zonal density gradient centrifugation, affinity chromatography, and nondenaturing electrophoresis of detergent-solubilized glyoxysomal and endoplasmic reticulum membranes consistently displayed 32- and 33-kDa silver-stained polypeptide bands, respectively.

Ricinus communis↗
PubMed1976

Aspects of the mechanism of action of local anesthetics on the sarcoplasmic reticulum of skeletal muscle.

1. The effect was studied of local anesthetics (tetracaine, dibucaine, procaine and xylocaine) on the forward and the backward reactions of the calcium pump of skeletal muscle sarcoplasmic reticulum. 2. The inhibition of the rate of calcium uptake, the rate of calcium-dependent ATP splitting and the rate of calcium-dependent ATP-ADP phosphate exchange by sarcoplasmic reticulum in the presence of the above drugs is at least partially due to the inhibition of the phosphoprotein formation from ATP. 3. The rate of the ADP-induced calcium release from sarcoplasmic reticulum and the rate of ATP synthesis driven by the calcium efflux are inhibited on account of a reduction of the phosphoprotein formation by orthophosphate. 4. The phosphorylation of calcium transport ATPase by either ATP or orthophosphate is diminished by the local anesthetics owing to a reduction in the apparent calcium affinity of sarcoplasmic reticulum emmbranes on the outside and on the inside, respectively. 5. The drug-induced calcium efflux from calcium-preloaded sarcoplasmic reticulum vesicles, a reaction not requiring ADP, is probably not mediated by calcium transport ATPase.

Adenosine Diphosphate↗