Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rat left atria or Langendorff hearts were kept at 37 degrees C and stimulated at a rate of 3.33 Hz. They were subjected to hypoxia (deprivation of oxygen) or ischemia (deprivation of oxygen and glucose + acidosis + increased extracellular potassium concentration) for 15 min or 1 h and subsequent reoxygenation for 5 or 15 min. Tissue concentrations of proteins, reduced and oxidized glutathione and conjugated dienes were measured at the end of the experiment. Hypoxia and ischemia decreased the excitability and contractility of the preparations and caused contracture. These effects were partly reversible during reoxygenation. However, in Langendorff hearts reoxygenation caused an increased release of CPK, LDH and glutathione into the perfusion fluid. Ischemia and reoxygenation in atria lowered the tissue concentration of reduced glutathione and increased its oxidized form. Similar changes were seen in atria and Langendorff hearts when oxygen radical production was accelerated by hypoxanthine and xanthine oxidase. No treatment raised significantly the concentration of conjugated dienes. These results seem to exclude an important role of an increased lipid peroxidation for reperfusion injury of isolated heart preparations.
J Mol Cell Cardiol 1989 Jul
PMID:No evidence for an increased lipid peroxidation during reoxygenation in Langendorff hearts and isolated atria of rats. 279 63

The behavior of cytoplasmic and mitochondrial enzymes has been studied in rat liver at 1, 5, and 24 hr after 60 min of ischemia using histochemical methods. This period of ischemia resulted 24 h after ischemia in liver cell necrosis in about 15% of the volume of the ischemic liver lobes. As early as after 1 hr reperfusion lactate dehydrogenase (LDH, cytoplasm) activity decreased in a certain proportion of the liver parenchymal cells, whereas glutamate dehydrogenase (GDH, mitochondrial matrix) activity started to decrease after 5 hr reperfusion; the activities of mitochondrial membrane enzymes, monoamine oxidase and succinate dehydrogenase, did not decrease before 24 hr of reperfusion. It has been concluded that the early decrease in LDH activity is caused by leakage into the blood and reflects reversible damage; when this decrease is accompanied by a decrease in GDH activity irreversible liver cell damage is assumed. Diminished activity of mitochondrial membrane enzymes, due to leakage and denaturation, is observed when real necrosis can be assessed.
Exp Mol Pathol 1987 Dec
PMID:Changes in cytoplasmic and mitochondrial enzymes in rat liver after ischemia followed by reperfusion. 367 63

The number of rat liver autophagic vacuoles (AVs) was increased by separate injection of three different inhibitors--vinblastine, leupeptin, and chloroquine--of lysosomal protein degradation. The different mechanisms of action of the agents correlated to the ultrastructure of the AVs. Accumulation of the base chloroquine with ensuing influx of water into AVs caused a significant swelling. The leupeptin-induced AVs were processed into residual-body-like structures within a few hours of exposure in line with the presence of a leupeptinase in liver tissue. Vinblastine was the most efficient agent in increasing the occurrence of AVs. The effect of vinblastine lasted for the entire study period (36 hr) with continuous formation of nascent AVs. In addition, vinblastine caused the appearance of a subpopulation of AVs laden with VLDL particles. The term crinosomes was suggested for these hybrid organelles, since they seemed to evolve by fusion between secretory granules and lysosomes. In addition to sequestered cell organelles, the AVs harbored cytosolic enzyme activities (LDH and aldolase). Leupeptin was the only agent that caused a decrease in cathepsin B and L activities. Similarly, leupeptin impeded protein breakdown in isolated AVs, whereas vinblastine and chloroquine evoked an increase. In vivo, chloroquine and vinblastine block protein degradation. The reason for this discrepancy is probably that during in vivo exposure the substrate (cytoplasmic proteins) is built up in the AVs because degradation is retarded. Upon isolation of the AVs the inhibitor block is released, and proteolysis proceeds at enhanced rates over control due to excess of substrates. Leupeptin, on the other hand, caused a substantial inhibition of thiol proteinases; this block remained in the isolated AVs. Accordingly, leupeptin-induced AVs displayed decreased protein degradation following shorter exposure times. Later, when leupeptin was metabolized, catch-up proteolysis was noted. The differing mechanisms of action of the inhibitors were also apparent as regards lipid contents and lipolysis. Whereas chloroquine and vinblastine increased the amounts of cholesterol and triglycerides parallel to proteins, leupeptin had no such effect. Lipolysis proceeded at normal rate following leupeptin administration, which was not the case after vinblastine and chloroquine exposure. Leupeptin has no effect on acid lipases; therefore lipids do not accumulate in AVs of hepatocytes that are exposed to leupeptin.
Exp Mol Pathol 1987 Dec
PMID:Comparison of different autophagic vacuoles with regard to ultrastructure, enzymatic composition, and degradation capacity--formation of crinosomes. 367 66

The role of cytosolic free Ca2+ (Caf) in cell injury was investigated using two methods for measuring Caf in freshly disaggregated embryonic chick heart cells. The null-point method, using arsenazo III, is based on determining the extracellular Ca2+ concentration at which no net Ca2+ movement occurs when plasma membrane permeability is increased. With this technique, the null point Caf averaged 0.23 +/- 0.07 microM (n = 6) in the basal state. Using quin2, an intracellular fluorescent dye, to measure Caf a value of 0.05 +/- 0.01 microM (n = 5) was obtained. Elevation of Caf by various agents was associated with an increase in cell injury as measured by the release of the cytosolic enzyme, LDH. However, the relationship between Caf and LDH release was not a direct one under all experimental conditions, indicating that the level of Caf is not the sole determinant of cell injury.
J Mol Cell Cardiol 1985 Mar
PMID:Cytosolic free calcium in chick heart cells. Its role in cell injury. 383 22

We show that the L-(+)-lactate dehydrogenase (EC 1.1.1.27;L-lactate: NAD+-oxidoreductase) of Plasmodium falciparum (LDH-P) is encoded in the parasite genome. A monoclonal antibody (McAb 7.2) has been shown to bind the LDH-P subunit which has an apparent molecular mass of 35 kDa. A polyclonal antiserum raised against affinity purified LDH-P has been used to isolate cDNA clones containing LDH-P epitopes from a lambda gt11Tn5 expression library. DNA sequence analysis of one clone, lambda LDH-P.1, reveals a single open reading frame which shows a degree of homology to the N-terminal domain of known LDH amino acid sequences.
Mol Biochem Parasitol 1985 May
PMID:Cloning studies on the gene coding for L-(+)-lactate dehydrogenase of Plasmodium falciparum. 389 92

A peptide bearing an antigenic determinant of the sperm-specific lactate dehydrogenase C4 isozyme (LDH-C4) has been isolated from a tryptic digest of the whole protein. This peptide, comprising residues 152-159 (MC152-159), reacts with rabbit anti-mouse LDH-C4. Immunization of rabbits with synthetic MC152-159 conjugated to bovine serum albumin induces an immune response which is specific for the peptide. Anti-MC152-159 IgG binds 125I-labeled mouse LDH-C4 and competition experiments demonstrate the specificity of this antigen antibody reaction.
Mol Immunol 1982 Dec
PMID:Identification of an antigenic determinant of mouse lactate dehydrogenase C4. 618 6

The activities of serum lactate dehydrogenase (S-LDH) and S-LDH isoenzymes were determined in 252 patients with a history of testicular germ cell tumors (TGCT). Fifteen of 37 patients with TGCT lesions and seven of 215 without had raised levels of S-LDH (above 8.0 mukat/l (480 U/l)). Of the patients with TGCT lesions, four had only raised S-LDH-1 levels, one only raised S-LDH-2 (and normal S-LDH), two only raised S-LDH-3 (one with normal S-LDH), and 10 had five combinations of raised levels of S-LDH isoenzymes with a predominance of S-LDH-1. S-LDH and S-LDH-1 correlated significantly with the total tumor volume in the patients with TGCT lesions, especially pronounced in those with lesions from seminoma. Of 34 patients with TGCT metastases, 13 with raised S-LDH levels lived significantly shorter lengths of time than 21 with normal S-LDH. Similarly, 11 with raised S-LDH-1 (above 3.0 mukat/l (180 U/l) lived significantly shorter times than 23 with normal S-LDH-1. S-LDH is a valuable tumor marker in patients with TGCT, especially in those with seminoma. Routine determination of S-LDH isoenzymes in addition to S-LDH in patients with TGCT is not recommended. In patients with a history of TGCT and an unexplained elevation of S-LDH levels, a raised S-LDH-1 level indicates the presence of TGCT lesions.
Mol Gen Genet 1983
PMID:Serum lactate dehydrogenase (S-LDH) and S-LDH isoenzymes in patients with testicular germ cell tumors. 619 72

A comparative study of the effect of temperature (10, 20, 30 and 37 degrees C) upon Km and V of alpha-hydroxyacid dehydrogenase (HADH), isozyme I and II, from Trypanosoma cruzi, a parasite whose life cycle comprises stages in an insect vector, and of another enzyme with analogous substrate specificity, the lactate dehydrogenase, isozyme X (LDH X) from mouse, a homeotherm, is presented. The Km for alpha-ketoisocaproate of HADH is markedly reduced as temperature decreases. This effect can compensate the reduction in thermal energy and produce stabilization of the reaction rate. This compensation does not occur with mouse LDH X. The activation energy for both HADH isozymes is about half the value determined for mouse LDH X. Results indicate that HADH from T. cruzi is able to adjust instantaneously to thermal changes of the environment, behaving as other enzymes of terrestrial poikilothermic animals.
Mol Biochem Parasitol 1984 Feb
PMID:Effect of temperature upon catalytic properties of alpha-hydroxyacid dehydrogenase from Trypanosoma cruzi. 636 42

An intact preparation of adult ventricular muscle cells was incubated in substrate-free, pH-constant, anoxic Tyrode solution. The time course of metabolic changes was found to depend on the relation of cell number to incubation volume: the smaller the volume, the faster anoxic damage develops. Energy needs decline rapidly during anoxia. Yet glycolytic energy production remains insufficient, since it also declines. Glycogenolysis stops after degradation of only half the glycogen present initially. Release of cytosolic enzymes (LDH, MDH) starts with the initial decrease in high-energy phosphates and proceeds correlated to the actual ATP content (r = -0.98) during the stage of reversible cell injury. An ATP content of 2 mumol/g wet wt. marks a critical threshold, below which more and more cells become irreversibly damaged. In the cell culture system, the anoxic process develops similarly to that of the oxygen deficient organ, however prolonged as in arrested hearts.
J Mol Cell Cardiol 1984 Nov
PMID:Energy metabolism and enzyme release of cultured adult rat heart muscle cells during anoxia. 639 66

At least two stages have been revealed in the reaction of enzymatic reduction of pyruvate under inhibition. A fast process during the first stage of the reaction was finished in a period of "dead time" with routine spectroscopic measurements. A reaction rate at this stage decreased by three times. The second stage was characterized by a constant rate, which changed by less than 10%. The analysis of neutral salt influences on the inhibition complex showed, that the latter decomposed rapidly. A model suggested earlier, was used for interpreting the reversible product inhibition of the reaction catalysed by LDH.
Mol Biol (Mosk)
PMID:[Biphase reaction of enzymatic pyruvate reduction during inhibition]. 647 64


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