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[Structural changes in Candida lipolytica cells during citric acid biosynthesis].

The techniques of light and electron microscopy were used to study structural changes in Candida lipolytica cells related to limitation of their growth and a nitrogen source in medium with glucose and hexadecane and transition of the culture to the production of citric acids. Changes in the content of protein in the cell and in the activities of enzymes of the citrate and glyoxylate cycles located in mitochondria and peroxysomes of the yeast were investigated at the same time. The results characterizing cytological changes in the cell of C. lipolytica in the conditions of citric acid biosynthesis fit in well with the data on protein content and enzyme activities in the cells obtained by biochemical analysis. The transition of the yeast cells to the overproduction of citric acids has been shown to be related to profound rearrangements of the cell: the inhibition of protein synthesis; changes in the structure of the cytoplasm; the appearance of vacuoles of an irregular shape, often in contact with the mitochondria; changes in the mitochondrial and peroxysomal apparatus; the accumulation of lipids. It has been demonstrated once again that the peroxysomal apparatus of the yeast cell has a relationship with the metabolism of n-alkanes.

Candida↗
PubMed1982

Functional and structural changes in veins in spontaneous hypertension.

Six month old spontaneously hypertensive rats (SHR) and age and sex matched normotensive Wistar-Kyoto rats (WKY) were examined to evaluate the existence of functional and structural changes in the portal vein (PV), inferior vena cavae (IVC) and pulmonary arteries (PA). PV, central nervous and systolic right ventricular pressures did not differ in the anesthetized SHR when compared with WKY, despite elevated systolic arterial pressure. PV, IVC and PA obtained from SHR were less extensible, developed more tension, exhibited an enhanced sensitivity to serotonin and a thromboxane-like prostanoid, accumulated more of the protein precursors 2-14C-leucine, 2-14C-glucosamine, 7-3H-fucose, exhibited a normal rate of uptake of 2-14C-thymidine, and increased protein content and a decreased concentration of DNA. When examined under light and electron microscopy, the veins and PA obtained from SHR demonstrated medial smooth muscle hypertrophy, and increased density of PAS-Schiff positive stain, enlarged and prominent Golgi apparati and an increased cell diameter through the region of the nucleus. These changes were not due to water-logging since the water content of the veins and PA from SHR and WKY did not differ. These data support the conclusion that PV, IC and PA obtained from SHR exhibit functional and structural changes independent of increases in intravenous pressure. These changes may relate to the increase in blood vessel protein.

Animals↗
PubMed1992

Structural changes and enhancements in DNase I footprinting experiments.

In footprinting experiments, an increase in DNA cleavage with addition of ligand to a system may be due to a ligand-induced structural change. Ligand binding also enhances cleavage by displacing the cleavage agent from ligand-binding sites, thus increasing its concentration elsewhere. The theory and characteristics of this mass-action enhancement are given, and it is shown how it may be recognized. Results of DNase I footprinting of small oligomers, with actinomycin D as ligand, are analyzed to reveal which enhancements are due to mass action, and which can reasonably be ascribed to structural changes. Patterns in the footprinting plots from our experiments on actinomycin D binding to a 139-base-pair DNA fragment (with DNase I as a probe) are studied in the same way. The likely origins of these patterns are discussed, as are enhancements occurring with other probes commonly used in footprinting experiments.

Base Sequence↗
PubMed1992

Glomerular structural changes in type 1 (insulin-dependent) diabetes mellitus: causes, consequences, and prevention.

Diabetic nephropathy is caused primarily by advanced glomerulopathy, the renal expression of diabetic microangiopathy. With stereological methods a quantitative description of the structural changes is achieved. The glomerulopathy is characterized by an increase in basement membrane material: thickening of the capillary wall and an increase in mesangial volume relative to glomerular volume, comprising increase in matrix. Among groups of patients conformity between renal function stage and structure exists. The parameters measuring glomerulopathy are normal at the onset of diabetes; patients with normoalbuminuria may show slight basement membrane thickening, or normal parameters; the microalbuminuric group shows a measurable, but moderate glomerulopathy; patients with overt nephropathy have advanced lesions; at this stage heterogeneity among glomeruli makes the estimates weaker. Recent data indicate that the changes in peripheral basement membrane and in mesangial matrix develop in concert and both contribute to the early stage of glomerulopathy in patients with microalbuminuria. As to the consequences of the structural changes the mechanism of albuminuria is not clear. It is suggested that the early glomerulopathy entails other structural modifications, including formation of new vessels which may be the site of leakage. The marked deviations in glomerular filtration rate correspond well with estimates of filtration surface area: in the early hyperfunction state it is increased; in advanced nephropathy it is decreased, due to advanced glomerulopathy in conjunction with glomerular occlusion. The diabetic state is the necessary condition for the glomerulopathy. In relating structural changes to presumed contributing causes no supporting evidence of a relationship with glomerular hyperfunction or hypertrophy was observed. The structural parameters may be useful tools in clinical trials aiming at arresting the development of glomerulopathy, and thereby providing a prevention of diabetic nephropathy.

Diabetes Mellitus, Type 1↗
PubMed1999

Structural change of threonine 89 upon photoisomerization in bacteriorhodopsin as revealed by polarized FTIR spectroscopy.

The all-trans to 13-cis photoisomerization of the retinal chromophore of bacteriorhodopsin occurs selectively, efficiently, and on an ultrafast time scale. The reaction is facilitated by the surrounding protein matrix which undergoes further structural changes during the proton-transporting reaction cycle. Low-temperature polarized Fourier transform infrared difference spectra between bacteriorhodopsin and the K intermediate provide the possibility to investigate such structural changes, by probing O-H and N-H stretching vibrations [Kandori, Kinoshita, Shichida, and Maeda (1998) J. Phys. Chem. B 102, 7899-7905]. The measurements of [3-18O]threonine-labeled bacteriorhodopsin revealed that one of the D2O-sensitive bands (2506 cm(-1) in bacteriorhodopsin and 2466 cm(-1) in the K intermediate, in D2O exhibited 18(O)-induced isotope shift. The O-H stretching vibrations of the threonine side chain correspond to 3378 cm(-1) in bacteriorhodopsin and to 3317 cm(-1) in the K intermediate, indicating that hydrogen bonding becomes stronger after the photoisomerization. The O-H stretch frequency of neat secondary alcohol is 3340-3355 cm(-1). The O-H stretch bands are preserved in the T46V, T90V, T142N, T178N, and T205V mutant proteins, but diminished in T89A and T89C, and slightly shifted in T89S. Thus, the observed O-H stretching vibration originates from Thr89. This is consistent with the atomic structure of this region, and the change of the S-H stretching vibration of the T89C mutant in the K intermediate [Kandori, Kinoshita, Shichida, Maeda, Needleman, and Lanyi (1998) J. Am. Chem. Soc. 120, 5828-5829]. We conclude that all-trans to 13-cis isomerization causes shortening of the hydrogen bond between the OH group of Thr89 and a carboxyl oxygen atom of Asp85.

Aspartic Acid↗
PubMed1987

The transducin cascade is involved in the light-induced structural changes observed by neutron diffraction on retinal rod outer segments.

Time-resolved neutron diffraction on retinal rod outer segments are performed to reinvestigate the origin of the light-induced structural change observed by Saibil et al. (Saibil, H., M. Chabre, and D. L. Worcester, 1976, Nature (Lond.), 262:266-270). Photoactivating rhodopsin triggers in rods a cascade of GTP-dependent and transducin-mediated reactions controlling cyclic-GMP hydrolysis. Infrared light-scattering studies (Kühn, H., N. Bennett, M. Michel-Villaz, and M. Chabre, 1981, Proc. Natl. Acad. Sci. USA, 78:6873-6877; Vuong, T. M., M. Chabre, and L. Stryer, 1984, Nature (Lond.), 311:659-661) demonstrated the existence of structural changes that correspond to this cascade rather than to rhodopsin photoactivation. We thus look for neutron diffraction changes of similar origins. With 1-min time resolution, intensity changes are observed mainly for orders 2 and 4. The illumination and GTP dependence of these changes indicates an involvement of transducin. Without GTP, they are linear with the amount of photoexcited rhodopsin, saturate at 10% photolysis, and thus correlate well with the light-scattering "binding signal." With GTP, light sensitivity is higher and saturation occurs below 0.5% photolysis, as for the "dissociation signal" of light scattering. In both cases, lattice compressions of 0.2-0.3% are observed. With 4-s time resolution the intensity change with GTP present precedes the lattice compression. The fast intensity change is probably due to the displacement of transducin alpha-subunits away from the disc membrane and the slower lattice shrinkage to an osmotic readjustment of the rod.

Animals↗
PubMed1986

Structural changes in reassembled growth plate aggregates.

To investigate possible structural changes in reassembled proteoglycan aggregates during cartilage mineralization, we examined the molecular architecture and dimensions of growth plate proteoglycan aggregates by electron microscopy. The ends of fetal bovine femurs and tibias were separated into three regions: the epiphysis; the cartilage growth plate, consisting of the proliferative zone and the unmineralized portion of the hypertrophic zone; and the calcified portion of the hypertrophic zone along with part of the metaphysis. Aggregates from all three regions had the same molecular architecture. They consisted of central hyaluronic filaments with multiple attached monomers. Monomers consisted of two segments: a peripheral thick segment, which represents primarily the chondroitin sulfate-rich region, and a thin segment attached directly to the hyaluronic acid filament. The length of aggregated monomers did not differ between the growth plate cartilage and the metaphysis, nor did the lengths of the thin and thick segments, indicating that the chondroitin sulfate-rich region of aggregated monomers is not degraded during cartilage mineralization. Between the growth plate cartilage and the metaphysis, aggregates became shorter and had fewer monomers and wider spacing between monomers. These structural alterations in proteoglycan aggregates may be one of the events that prepares the matrix for mineralization.

Animals↗
PubMed2002

Structural change of site-directed mutants of PYP: new dynamics during pR state.

The energetics, protein dynamics, and diffusion coefficients of three mutants of photoactive yellow protein, R52Q, P68A, and W119G, were studied by the transient grating and pulsed laser-induced photoacoustic method. We observed a new dynamics with a lifetime of approximately 1 micro s in the transient grating signal, which is silent by the light absorption technique. This fact indicates that, after the structure change around the chromophore is completed (pR(1)), the protein part located far from the chromophore is still moving to finally create another pR (pR(2)) species, which can transform to the next intermediate, pB. Although the kinetics of pR(2)-->pB-->pG are very different depending on the mutants, the enthalpies of the first long-lived (in micro seconds, 100-micro s range) intermediate species (pR(2)) are similar and very high for all mutants. The diffusion coefficients of the parent (pG) and pB species of the mutants are also similar to that of the wild-type photoactive yellow protein. From the temperature dependence of the volume change, the difference in the thermal expansion coefficients taken as indicator of the flexibility of the structure between pG and pR(2) is measured. They are also similar to that of the wild-type photoactive yellow protein. These results suggest that the protein structures of pR(2) and pB in these mutants are globally different from that of pG, and this structural change is not altered so much by the single amino acid residue mutation. This is consistent with the partially unfolded nature of these intermediate species. On the other hand, the volume changes during pR(1)-->pR(2) are sensitive to the mutations, which may suggest that the volume change reflects a rather local character of the structure, such as the chromophore-protein interaction.

Acoustics↗
PubMed1988

Localized melting and structural changes in the SV40 origin of replication induced by T-antigen.

Replication of simian virus 40 (SV40) DNA is dependent upon the binding of the viral T-antigen to the SV40 origin of replication. Structural changes in the origin of replication induced by binding of T-antigen were probed by chemical modifications of the DNA. In the presence of ATP, T-antigen rendered two of three domains in the SV40 core origin hypersensitive to attack by either dimethyl sulfate or potassium permanganate (KMnO4). One of these domains, the early palindrome, was shown to contain an 8-bp region of melted DNA as determined from methylation of cytosine residues and by nuclease S1 cleavage of methylated DNA. DNA melting was not dependent upon either the hydrolysis of ATP or the binding of T-antigen to an adjacent site (site I). A second domain, the A/T element, was extensively modified by KMnO4 but no significant melting was detected. Rather, the pattern of modification indicates that T-antigen caused a conformational change of the double-stranded DNA in this region. These results suggest that T-antigen, in the presence of ATP, destabilizes the SV40 origin by melting and structurally deforming two flanking regions within the core origin sequence. These DNA structural changes may provide access to other replication factors, allowing complete denaturation of the SV40 origin and the initiation of SV40 DNA replication.

Adenosine Triphosphate↗
PubMed1995

A comparison of the effect of angiotensin converting enzyme inhibition and angiotensin II receptor antagonism on the structural changes associated with hypertension in rat small arteries.

OBJECTIVE: To investigate whether, when angiotensin converting enzyme inhibitors are administered to young, genetically hypertension-prone animals, the demonstrated attenuation of blood pressure development and prevention of the structural changes usually observed in small arteries is attributable to the prevention of angiotensin II production. DESIGN: We have treated spontaneously hypertensive rats (SHR) aged 4-20 weeks with either lisinopril (1 or 10 mg/kg) or the angiotensin II receptor antagonist D 8731 (1, 20 or 50 mg/kg). METHODS: Blood pressure was measured and structural parameters in small arteries from four vascular beds were examined using isometric myography. RESULTS: At age 20 weeks lisinopril had attenuated blood pressure development and prevented cardiac hypertrophy (but not vascular hypertrophy) in a dose-dependent manner. The highest dose of lisinopril had reduced the blood pressure of the SHR to below that of the Wistar-Kyoto (WKY) rats and prevented most structural changes, but there was a slight reduction in body weight in those rats. Comparable blood pressure control with D 8731 was associated with similar structural parameters. CONCLUSION: The prevention of hypertension-associated vascular structural alteration appears to be dependent upon the degree of blood pressure control.

Angiotensin Receptor Antagonists↗
PubMed1981

Structural changes in synthetic myosin minifilaments and their dissociation by adenosine triphosphate and pyrophosphate.

Morphologically similar short myosin and rod filaments (minifilaments) have been prepared in 10 mM Tris--citrate buffer, pH 8.0, in the absence of other myosin or rod forms. Both minifilament systems are dissociated in the same manner in the presence of ATP or pyrophosphate. Identical binding of these ligands to myosin and rod minifilaments suggests that myosin heads play no role in substrate-induced destabilization of the minifilaments. The effects of ATP and pyrophosphate on minifilaments are similar to their dissociating effect on synthetic filaments [Harrington, W. F., & Himmelfarb, S. (1972) Biochemistry 11, 2945--2952], thus justifying their use in conformational studies in lieu of filaments. In view of their small size and homogeneity, the minifilaments constitute an appropriate material for such studies. The binding of pyrophosphate to myosin and rod minifilaments decreases their alpha-helical content, as measured by circular dichroism. No change in the secondary structure of subfragment 1 and light meromyosin is observed upon binding of pyrophosphate, but substantial changes (10%) are detected in subfragment 2. The structural changes in myosin, possibly relevant to contraction, are localized in the subfragment 2 region of the molecule. These results emphasize the importance of charge interactions in the functional behavior of thick filaments.

Adenosine Triphosphate↗
PubMed2000

Difference in structural change in the Carpentier-Edwards pericardial valves implanted in the mitral and tricuspid positions.

We report a 29-year-old patient with prosthetic valve dysfunction with severe calcific stenosis in the mitral position but no structural change in the tricuspid position after mitral valve replacement and tricuspid valve supra-annular implantation with same bioprostheses at the seven years before. The difference in structural change between the mitral position and the tricuspid position might be due mainly to the effect of mechanical stress on the cusps, rather than to any difference in serum calcium levels. However, some hormonal effect other than that of the parathyroid hormone on the systemic and pulmonary circulation might be related to the early progression in cusp calcification in the systemic circulation.

Adult↗
PubMed1984

Early structural changes in precapillary vessels in hypertension and their relationship to functional changes.

This presentation has reviewed evidence from our laboratory that both structural and functional changes participate in the initiation and maintenance of hypertension in spontaneously hypertensive rats (SHR). Structural changes are present in the muscular arteries of the mesenteric and renal vasculature at 3- to 5-week-old SHR as compared with WKY. The major structural change in SHR arteries was increased cross-section area with increased thickness of the media owing to hyperplasia of smooth muscle; lumen sizes were interchanged. Later, at 10-12, 21, and 28 weeks of age, there was further increase in medial thickness owing to hyperplasia, and some hypertrophy and changes in elastic arteries also became evident. Increases in medial thickness of elastic arteries included hypertrophy as well as hyperplasia. Changes in lumen diameter were never observed in arteries fixed in a relaxed state at physiological flow rates. In addition, a deficit in Ca handling (decreased ATP-dependent Ca2+ accumulation) was observed in plasma-membrane vesicles from mesenteric arteries of SHR prior to and after the development of hypertension. It persisted when hypertension was reversed by hydralazine in SHR. It was present in various forms of experimental hypertension. It was present whenever hypertension was present and disappeared with normalization of blood pressure by withdrawal of the stimulus. The Ca-handling deficit was found in several nonarterial tissues and may be a generalized genetic defect in SHR. It was always accompanied by increased alkaline phosphatase activity of plasma membranes, and this was suggested to reflect the smooth-muscle hyperplasia occurring simultaneously. A model of the initiation and maintenance of hypertension based on medial thickening and deficient Ca handling as primary, interacting causes of genetic hypertension is proposed.

Animals↗
PubMed1976

Structural changes occurring during atresia in sheep ovarian follicles.

The structural changes that characterize primary, secondary and tertiary atresia in sheep Graafian follicles have been studied by means of histological, histochemical and ultrastructural techniques. In primary atresia vacuoles representing swollen endoplasmic reticulum are prominent along the antral border together with disorganized granulosa cells containing pyknotic nuclei. Phagocytic cells, which increase in number as atresia progresses, were seen within the membrana granulosa and are considered to be transformed granulosa cells. Even in follicles classified as nonatretic, a few antral vacuoles and occasional pyknotic nuclei are present. During secondary atresia there is a large increase in the number of cells with pyknotic nuclei; many of these nuclei had been extruded and had fused to form the characteristic Feulgen-positive atretic bodies found along the edge of the antral cavity. These bodies usually have a diameter of up to 15 mum but occasionally reached as much as 400 mum. A second area of degeneration is frequently present in the membrana granulosa, two or three cell layers from the basal lamina, and it is at this level that exfoliation of granulosa cells occurs in tertiary atresia. In contrast to the membrana granulosa, there are during secondary atresia, only slight indications of degeneration in the cumulus. In tertiary atresia the membrana granulosa is highly disorganized; the atretic bodies are often fewer in number than at earlier stages. The basal lamina remains essentially intact. It is at this stage that the first clear signs of degeneration occur in the theca interna. Despite some disintegration of the cumulus, the integrity of the oocyte is maintained and its nucleus remains vesicular. Changes in the thecal microcirculation may plan a key role in atresia: adjacent to the basal lamina of non-atretic follicles, there is a well-developed capillary network which is significantly reduced as atresia progresses.

Animals↗
PubMed1983

Structural changes of isolated hepatocytes during treatment with digitonin.

The structural changes accompanying digitonin-induced release of enzymes and metabolites from isolated hepatocytes have been studied by scanning and transmission electron microscopy. In the initial phase, characterized by total release of the cytosolic marker enzyme, lactate dehydrogenase, the plasma membrane was immediately damaged, rapidly followed by extensive damage to the endoplasmic reticulum. The shape of the cell, however, was maintained, and the mitochondria and nucleus remained tightly held together by the cytoskeleton. Mitochondria remained intact initially, whereas the cytosol became less electron dense and the nuclear chromatin was more dispersed. An intermediate phase was characterized by total release of adenylate kinase and most of the glucose-6-phosphatase, marker enzymes for the mitochondrial intermembrane space and the endoplasmic reticulum, respectively. The outer mitochondrial membrane was ruptured, but mitochondria maintained their normal matrix electron density. In the final phase, characterized by the beginning of citrate synthase release from the mitochondrial matrix space, the mitochondria became swollen, and only the nucleus, inner and outer mitochondrial membranes, and the cytoskeleton could be clearly distinguished. Although the plasma membrane could not be readily discerned in electron micrographs after the initial phase, the plasma membrane marker enzyme 5'-nucleotidase remained associated with digitonin-treated hepatocytes. Acetyl-CoA carboxylase was released much more slowly than lactate dehydrogenase, indicating some severe restriction on its release. The release of acetyl-CoA carboxylase closely paralleled the release of glucose-6-phosphatase. The controlled exposure of hepatocytes to digitonin, therefore, leads to the sequential release of soluble, compartmentalized cellular components and some membrane-bound components, but the mitochondrial membrane, cytoskeleton and the nucleoskeleton survive even long-term digitonin treatment.

Acetyl-CoA Carboxylase↗
PubMed1997

Structural changes in the aorta of the hereditary hypertriglyceridemic rat.

Structural changes in the ascending thoracic aorta of hereditary hypertriglyceridemic (hHTG), insulin-resistant, and hypertensive rats were studied using transmission electron microscopy. Normotensive Wistar rats were used as controls. The most-pronounced morphological changes were observed in the tunica intima. Endothelial cells of hHTG rats formed a continual layer around the whole circumference. Subendothelial space was enlarged. Some endothelial cells were delaminated from the subendothelial space by big lipid droplets that were often present in the subendothelial space, and the endothelial cells bulged out towards the lumen. Big electron-lucent lipid droplets were present in the majority of the endothelial cells and occupied the main part of the cytoplasm. Degenerative microvesicular and membranous material was present in the cytoplasm. Increased numbers of vesicles of Golgi apparatus and cisternae of endoplasmic reticulum were found. Similar morphological alterations, but in less-extended form, were observed in smooth muscle cells. The organization and orientation of smooth muscle cells were essentially intact. In muscle cells, lipid droplets were localized in close relation to Golgi complex and in dilated cisternae of the sarcoplasmic reticulum. Lipid droplets, degenerative material, myelin figures, myelinoid membranes, and vesicular components were also sporadically found in the intercellular space among muscle cells. This pilot morphological investigation provides further arguments for a thorough and more-focused electron microscopy study of conductance arteries of the hHTG rats.

Animals↗
PubMed2002

Experimental diabetes induces functional and structural changes in the peritoneum.

BACKGROUND: Peritoneal dialysis (PD) is an established renal replacement therapy in diabetic patients, but the influence of diabetes on the peritoneal membrane (PM) remains debated. We have used functional, biochemical and molecular studies in vivo and in vitro to substantiate the changes induced by diabetes and hyperglycemia in the PM. METHODS: Peritoneal equilibration tests were performed 2, 4, and 6 weeks after induction of diabetes with streptozotocin (STZ) in rats. Morphological analyses, determination of nitric oxide synthase (NOS) activities, and expression studies for NOS isoforms and advanced glycation end products (AGE) were performed in parallel. Additional studies were conducted in diabetic rats treated with insulin, non-diabetic rats fed with urea, and cultured bovine aortic endothelial cells (BAEC). RESULTS: In comparison with controls, diabetic rats were characterized by: increased permeability for small solutes and decreased sodium sieving; capillary proliferation; increased endothelial NOS (eNOS) and AGE immunoreactivity; up-regulation of eNOS and down-regulation of neuronal NOS; and increased NOS activity in the PM. The changes, which culminated at week 6, were prevented by chronic insulin treatment in diabetic rats. In contrast to hyperglycemia, hyperosmolality alone did not induce functional or structural changes in the PM. Studies in BAEC showed that high glucose incubation led to increased activity and expression of eNOS, a prerequisite for vascular proliferation. CONCLUSIONS: These data demonstrate that chronic hyperglycemia is associated with functional and structural changes in the peritoneum that parallel with selective regulation of NOS isoforms and AGE deposits. The alterations are prevented by insulin treatment, which suggests that adequate control of diabetes can preserve PM integrity in diabetic patients prior to PD.

Animals↗