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Query: EC:1.3.5.1 (
succinate dehydrogenase
)
8,177
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Chronic intraperitoneal injection of cadmium and copper salts produces cardiotoxic effects of various degree. The degree of the muscular tissue lesion in the ventricles and atria is inverse to the number of luminescent nervous terminals. Changes in the adrenergic fibers are accompanied with certain metabolic shifts in the muscular tissue of the heart; this is evident from decreasing
succinate dehydrogenase
activity in cardiomyocytes and accumulation of lipids. Certain disorders are also revealed in cardiomyocytes, in vessels and in interstitial connective tissue demonstrated as: plethora, phenomena of stasis in the capillary bed, moderate perivascular edema, myocardial dystrophy. The foci of lesions are found more often in the left ventricle in myocardial tissue and under epicardium, sometimes near plethoric vessels and less often in the right ventricle and in the atria. The dependence between location of the myocardial lesions and vascular disorders is not always noted. This is observed more often under effect of cadmium sulfate and, evidently, is dependent not only on hypoxia, connected with congestive plethora, but with neurohumoral influences, too.
Arkh Anat Gistol Embriol 1988
Sep
PMID:[Adrenergic innervation of the myocardium in rats with toxic exposures]. 321 69
A method has been developed for the histochemical demonstration of a variety of dehydrogenases in freeze-dried or fixed resin-embedded tissue. Seven dehydrogenases were studied. Lactate dehydrogenase, NADH dehydrogenase and NADPH tetrazolium reductase were all demonstrable in sections of paraformaldehyde-fixed resin-embedded tissue. Freeze-dried specimens were embedded, without fixation, in glycol methacrylate resin or LR Gold resin at either 4 degrees C or -20 degrees C. All the dehydrogenases except
succinate dehydrogenase
retained their activity in freeze-dried, resin-embedded tissue. Enzyme activity was maximally preserved by embedding the freeze-dried tissue specimens in glycol methacrylate resin at -20 degrees C. The dehydrogenases were accurately localized without any diffusion when the tissue sections were incubated in aqueous media. Addition of a colloid stabilizer to the incubating medium was not required. Freeze-drying combined with low-temperature resin embedding permits accurate enzyme localization without diffusion, maintenance of enzyme activity and excellent tissue morphology.
Histochem J 1988
Sep
PMID:Dehydrogenase enzyme histochemistry on freeze-dried or fixed resin-embedded tissue. 324 Sep 50
The effects of acetylsalicylic acid (ASA) at a dose of 800 micrograms/day per rat for 7 days on some androgenic parameters such as organ weights,
succinate dehydrogenase
, acid phosphatase, fructose, cholesterol and protein of testis, epididymis, vas deferens and accesory glands in adolescent male rats were investigated. The semen characteristics and scanning electron microscopy (SEM) study on sperm morphology of cauda epididymis were also carried out. The results revealed that the treatment manifested a marked effect in altering the metabolism of testis, cauda epididymis, seminal vesicle and vas deferens. The androgen antagonistic and antianabolic effects were by and large transient and reversible by ascorbic acid administration.
Endocrinol Exp 1988
Sep
PMID:Effects of acetylsalicylic acid on reproductive organs of adolescent male rats. 326 82
The replication initiator protein of bacteriophage f1 (gene II protein) binds to the phage origin and forms two complexes that are separable by polyacrylamide gel electrophoresis. Complex I is formed at low gene II protein concentrations, and shows protection from DNase I of about 25 base-pairs (from position +2 to +28 relative to the nicking site) at the center of the minimal origin sequence. Complex II is produced at higher concentrations of the protein, and has about 40 base-pairs (from -7 to +33) protected. On the basis of gel mobility,
complex II
appears to contain twice the amount of gene II protein as does complex I. The 40 base-pair sequence protected in
complex II
corresponds to the minimal origin sequence as determined by in-vivo analyses. The central 15 base-pair sequence (from +6 to +20) of the minimal origin consists of two repeats in inverted orientation. This sequence, when cloned into a plasmid, can form complex I, but not
complex II
. We call this 15 base-pair element the core binding sequence for gene II protein. Methylation interference with the formation of complex I by the wild-type origin indicates that gene II protein contacts six guanine residues located in a symmetric configuration within the core binding sequence. Formation of
complex II
requires, in addition to the core binding sequence, the adjacent ten base-pair sequence on the right containing a third homologous repeat. A methylation interference experiment performed on
complex II
indicates that gene II protein interacts homologously with the three repeats. In
complex II
, gene II protein protects from DNase I digestion not only ten base-pairs on the right but also ten base-pairs on the left of the sequence that is protected in complex I. Footprint analyses of various deletion mutants indicate that the left-most ten base-pairs are protected regardless of their sequence. The site of nicking by gene II protein is located within this region. A model is presented for the binding reaction involving both protein-DNA and protein-protein interactions.
J Mol Biol 1987
Sep
20
PMID:Interaction between the replication origin and the initiator protein of the filamentous phage f1. Binding occurs in two steps. 350 Mar 17
Poly- and monoclonal antibodies to neoantigens of the human C5b-9 complement complex, as well as polyclonal antibodies to C5, C8, and C9, were used to detect and identify C5b-9 deposits in human myocardial tissue. Immunocytochemical studies were performed on fresh-frozen autopsy material derived from patients with myocardial infarctions; in addition, in 17 of these patients, paraffin sections of formalin-fixed tissue were investigated. Sixteen autopsies from patients with noncardiac diseases were analyzed as controls. Without exception, C5b-9 positivity was registered selectively and exclusively on and in myocardial cells located within the zones of infarction. The selectivity of staining was confirmed by control reactions for
succinic dehydrogenase
activity performed in adjacent, respective double-stained sections. Most intensive staining with anti-neoantigen antibodies was observed in the peripheral areas of the infarctions. Weak staining for C3d, rather strong staining for C5 and C9, and intermediate staining with anti-C8 antibodies were observed in the same localizations. Stainings for C4 and IgA were negative, whereas immunocytochemical reactions for IgG and IgM revealed an irregular and very weak staining. Only very weak staining was also observed with a monoclonal antibody to complement S-protein, indicating that the terminal complement components were deposited mainly in the form of membrane-damaging C5b-9 complexes. Immunocytochemical staining for C5b-9 was found to represent a most sensitive tool for detection of ischemic myocardial lesions, permitting easy detection even of single cell necroses. As a working hypothesis, we suggest that initial ischemia may cause loss of the ability of the heart muscle cells to regulate complement turnover at the membrane level. The resulting deposition of C5b-9 on the cell membranes may contribute to functional disturbance and irreversible damage of myocardial cells during the infarction process.
J Immunol 1986
Sep
15
PMID:Deposition of the terminal C5b-9 complement complex in infarcted areas of human myocardium. 352 91
Anion exchange plays an important role in renal ion transport and acidification. To further understand the molecular nature of renal epithelial anion exchange, we used a monoclonal antibody to the membrane domain (52 kDa) of human erythrocyte band 3 protein to immunocytochemically search for this polypeptide in the rabbit kidney. In cryostat sections, a subpopulation of cells in the cortical and outer medullary collecting tubules showed immunoreactivity; labeling was restricted to the basolateral membrane. Proximal tubules and thick and thin limbs of Henle showed no immunoreactivity. Approximately 11% of cells in the cortical, but 43% of cells in the medullary, collecting tubule were positive for band 3. To determine the type of cells that were band 3 positive, mitochondria-rich (intercalated) cells were identified by their positive histochemical staining for
succinic dehydrogenase
activity and by their ability to bind peanut lectin at the apical membrane. In the cortical collecting tubule, the majority of mitochondria-rich cells bound peanut lectin but were band 3 negative; the remainder were band 3 positive but lectin negative. This distribution was reversed in the inner stripe of the outer medulla: all mitochondria-rich cells were band 3 positive and lectin negative. Thus mitochondria-rich cells are of at least two types, each of which has a distinct axial distribution pattern. Given available information about in vitro HCO3 transport properties of rabbit collecting tubules, it is likely that the lectin-positive, band 3-negative mitochondria-rich cells secrete HCO3, whereas the lectin-negative, band 3-positive cells reabsorb HCO3 (secrete H).
Am J Physiol 1986
Sep
PMID:Two types of collecting duct mitochondria-rich (intercalated) cells: lectin and band 3 cytochemistry. 352 79
1. Long-term electrical stimulation was given to the peroneal nerve of deafferented hindlimbs in hemispinalized adult cats. The amount of stimulation covered 0.5-5.5% of total time per day, different in different animals. For some aspects of the present study, use was also made of cats subjected to "tonic" patterns of chronic stimulation (typically covering 50% of total time; 10, 16). 2. In a terminal acute experiment under general anesthesia, performed after 4 or 8 wk of long-term stimulation, one of the treated peroneal muscles (m. peroneus longus, PerL) was used for measurements of the resistance to contractile fatigue. The fatigue test consisted of 0.33-s bursts of motor-nerve stimulation at 40 Hz, repeated once a second for 4 min (6, 7). During this fatigue test, the evoked compound spikes of the muscle were recorded by electromyographic (EMG) techniques. Following the physiological procedures, PerL was removed for further histochemical analysis. In transverse sections, measurements of optical density were made in central regions of single fibers after staining for the activity of an oxidative enzyme,
succinate dehydrogenase
(core SDH). 3. Findings from chronically stimulated PerL muscles were compared with three kinds of control PerL muscles: 1) those contralateral to the stimulated ones, 2) those from the operated side of animals that had been deafferented and hemispinalized but not subjected to chronic stimulation, and 3) those from untreated normal animals. 4. Stimulation patterns covering both greater than or equal to 50% and 5-5.5% of daily time gave a marked improvement of fatigue resistance. Pulse rate seemed of little importance for these effects. The pattern covering only 0.5% of total daily time caused no increase of contractile endurance beyond that of normal muscles. 5. During the fatigue test of a control muscle (see above), the amplitude of the compound EMG spikes typically showed a marked decline. This "EMG depression" was effectively counteracted by all the present patterns of chronic stimulation, including the 0.5% pattern. 6. Fibers of chronically stimulated muscles became more similar to each other with respect to their density of core SDH staining. However, among muscles treated during 0.5-5.5% of total daily time, the degree and pattern of change in core SDH staining was not related to the amount and pattern of chronic stimulation or to the resulting degree of contractile endurance.
J Neurophysiol 1987
Sep
PMID:Effects of physiological amounts of high- and low-rate chronic stimulation on fast-twitch muscle of the cat hindlimb. II. Endurance-related properties. 365 85
Young rats exposed to an odor while receiving reinforcing stimulation come to approach that odor upon subsequent presentation. In addition, such pups have increased 14C-2-deoxyglucose (2DG) uptake within focal areas of the glomerular layer in response to that odor, compared to control animals experiencing the odor for the first time. In this study, the morphology of the glomerular areas underlying these 2DG foci was examined to determine whether early olfactory learning imposed local structural changes that could produce the enhanced 2DG uptake. Alternate sections either were processed with a silver and a Nissl stain to label both cell bodies and their processes or were histochemically treated for the mitochondrial enzymes cytochrome oxidase (CO) or
succinic dehydrogenase
(
SDH
) to define the glomerular core of the bulb; 2DG autoradiographs were aligned with adjacent stained sections, and regions underlying the high 2DG uptake foci were examined. In odor-familiar animals, large glomerular clusters that protruded into the external plexiform layer or the olfactory nerve layer were associated with the focal areas of increased 2DG uptake. Morphometric analysis of these regions revealed that the glomerular layer underlying the foci of high 2DG uptake was 30% wider in odor-familiar animals than comparable areas in odor-unfamiliar animals; the cross-sectional areas of individual glomeruli were 21% larger in odor-familiar animals. The foci of enhanced 2DG uptake therefore appear to be associated with groups of enlarged glomeruli. These data demonstrate that early olfactory learning influences the morphology of the olfactory bulb.
J Comp Neurol 1987
Sep
01
PMID:Localized changes in olfactory bulb morphology associated with early olfactory learning. 366 67
The effect of severe protein deprivation and subsequent nutritional rehabilitation on the fibre size and mitochondrial enzyme activity of the extensor digitorum longus (EDL) and soleus muscles of the young rat has been examined. Protein deprived rats showed atrophy of type 2 fibres predominantly, reduced histochemical activity of
succinic dehydrogenase
(
SDH
) and reduced biochemical activity of citrate synthase. Nutritional rehabilitation indicated by resumption of the original body weight resulted in complete restitution of the weight of the muscles and the size of type 1 and type 2 fibres, but not of the activity of
SDH
and citrate synthase. The results indicate that regarding size, type 2 fibres tend to be more influenced than type 1 fibres by the nutritional supply. The mitochondrial enzyme activity which is decreased by protein deprivation does not regain the normal levels as quickly as the muscle fibres resume their normal size.
J Neurol Sci 1986
Sep
PMID:Nutritional rehabilitation of skeletal muscle in protein-deprived young rats. 376 Sep 9
The consequence of blocking the de novo synthesis of ubiquinone (coenzyme Q) on mitochondrial ubiquinone content and respiratory function was studied in cultured C1300 (Neuro 2A) murine neuroblastoma cells. Mevinolin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, was used to suppress the synthesis of mevalonate, an essential precursor for the isoprenoid side chain of ubiquinone. At a concentration of 25 microM, mevinolin completely inhibited the incorporation of [3H]acetate into ubiquinone, isolated from cell extracts by two-dimensional thin-layer chromatography. Similar results were obtained when [14C]tyrosine was used as a precursor for the quinone ring. Through the use of reverse-phase thin-layer chromatography, it was established that the principal product of the ubiquinone pathway in murine neuroblastoma cells was ubiquinone-9. Inhibition of ubiquinone synthesis for 24h in cells cultured in the presence of 10% fetal calf serum (which contains 0.14 nmol of ubiquinone/ml of serum) resulted in a 40-57% decline in the concentration of ubiquinone in the mitochondria. However, the activities of succinate-cytochrome c reductase and
succinate dehydrogenase
in whole-cell homogenates or mitochondria were not inhibited. The state 3 and uncoupled rates of respiration, determined by polarographic measurements of oxygen consumption in homogenates and mitochondria, were elevated slightly in the mevinolin-treated cells. The data demonstrate that, although mevalonate synthesis is important for the maintenance of the intramitochondrial ubiquinone pool in cultured cells, major changes in the ubiquinone content of the mitochondria can occur in intact cells without perturbation of respiratory function. However, the coincidence of decreased mitochondrial ubiquinone concentration and the inhibition of cell cycling previously observed in mevinolin-treated cells (Maltese, W.A. (1984) Biochem. Biophys. Res. Commun. 120, 454-460) suggests that the availability of ubiquinone may play a role in the regulation of mitochondrial and cellular proliferation.
J Biol Chem 1985
Sep
25
PMID:Relation of mevalonate synthesis to mitochondrial ubiquinone content and respiratory function in cultured neuroblastoma cells. 385 88
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