Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:1.6.99.3 (diaphorase)
5,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rabbits being repeatedly poisoned with small doses of sodium cyanide, the activity of succinic dehydrogenase in the tissues does not essentially change. The activity of NAD.H2-cytochrome-c-reductase and NAD.H2-diaphorase in the brain, myocardium and kidneys increases. Under histotoxic hypoxia the level of iron in the tissues increases by 52-93%, that of copper--by 28-36%, of zinc--by 21-74% and of cobalt by 28-40%. There existed a positive correlation between the content of iron and the activity of NAD-dependent enzymes. In nonlethal form of histotoxic hypoxia the content of nonhemin iron and the activity of NAD.H2-cytochrome-c-reductase in the mitochondria of the brain increases by 25% and 17%, respectively, and a direct correlation is revealed between them.
...
PMID:[Iron, copper, zinc and cobalt content and activity of respiratory metalloenzymes in animal tissues under toxic hypoxia]. 68 69

Zinc deficiency (ZD) is teratogenic in rats, and fetal skeletal defects are prominent. To elucidate further the effects of maternal ZD in the fetal skeleton, we performed a morphological and histochemical study of tibial growth plate (GP) in ZD rat fetuses. The histochemical study included the identification of calcium, of hydrolytic enzymes associated with the process of calcification, and of oxidative enzymes related to energy production and to the synthesis of proteoglycans. Pregnant Sprague-Dawley rats were fed (1) a control diet (76.4 micrograms Zn/g diet) ad libitum (group C), (2) a zinc-deficient diet (0 micrograms/g) ad libitum (group ZD), or (3) the control diet pair-fed to the ZD rats (group PF). On day 21 of gestation, laparotomies were performed, the fetuses were removed, and fetal tibiae obtained. Specimens were stained with hematoxylin-eosin (H&E) and Masson Trichrome and were processed for identification of alkaline phosphatase, adenosine triphosphatase, succinic dehydrogenase, NADH dehydrogenase, and calcium. The morphologic patterns found in ZD fetal tibiae indicated defects in various cell types implicated in bone metabolism. Staining for hydrolytic enzymes revealed alterations in the size and distribution of matrix vesicles and a weaker staining for ATPase in ZD fetuses. Staining for oxidative enzymes was overall more intense in ZD fetal tibiae. ZD fetuses also presented irregular and defective calcification. These findings indicate that severe maternal ZD in the rat results in structural and functional alterations in the GP of fetal bone, leading to a defective endochondral ossification.
...
PMID:Changes in the fetal tibial growth plate secondary to maternal zinc deficiency in the rat: a histological and histochemical study. 196 89

Slow waves in the small intestine seem to arise in plexuses of neurites with interstitial cells of Cajal. In the colon, slow waves appear to arise at the circular muscle - submucosal interface. We therefore sought a plexus at this surface in the colon in the cat, dog, ferret, opossum, rabbit, rat, guinea-pig and man. Segments from all levels of the colon were stained by the Champy-Maillet osmic acid-zinc iodide method and cut into serial 25 micron sections in the plane of the muscle layers. A dense network of neurites with abundant interstitial cells of Cajal was found at the circular muscle - submucosal interface in all species except rabbit. Neurites in this plexus appeared to arise from the deep plexus of the submucosa (Schabadasch's or Henle's plexus). It was not found in the small intestine and stomach. A similar plexus was found in the interstices of the myenteric plexus in the colon. Interstitial cells of Cajal in both plexuses were positive for the NADH-diaphorase stain, but not for silver impregnation. The possible roles of the plexuses of neurites and interstitial cells of Cajal at the circular muscle - submucosal interface and at the plane of the myenteric plexus in the generation of rhythmic activity in the colon are discussed.
...
PMID:Intrinsic nerves in the mammalian colon: confirmation of a plexus at the circular muscle-submucosal interface. 245 50

The influence of dietary iron deficiency, lead exposure or their combination on certain enzymes, and the accumulation of Pb and essential metal levels in vital organs of rats was investigated. Iron deficiency caused alterations in the activity of muscle, hepatic and renal succinate dehydrogenase, and hepatic mitochondrial succinate cytochrome c reductase, whereas Pb exposure had no influence on these enzymes. There was no synergistic effect of the two factors on the activity of the enzymes. However, feeding of a Fe-deficient diet during Pb exposure enhanced the accumulation of Pb in soft tissues and flat bones. The hepatic copper and zinc levels were lowered upon either feeding a Fe-deficient diet or Pb exposure. However, the synergistic effect of the two factors was evident in hepatic Cu, but not in hepatic Zn. The feeding of a Fe-deficient diet decreased liver, kidney, and spleen levels of Fe, whereas Pb exposure decreased kidney and spleen Fe. The synergistic influence of the two factors could be observed only in liver and kidney.
...
PMID:Interrelationship between iron deficiency and lead intoxication (Part 2). 248 15

Recent studies have suggested that large amounts of free zinc may be coreleased during excitatory synaptic transmission at glutamatergic synapses, and may act postsynaptically to decrease actions mediated by N-methyl-D-aspartate (NMDA) receptors, while often increasing neuroexcitation mediated by quisqualate receptors. The present study examined the ability of zinc to alter excitatory amino acid (EAA) neurotoxicity. Murine cortical cell cultures were exposed to EAAs for 5 min in defined solutions, and neuronal cell injury was examined the following day both morphologically and by lactate dehydrogenase assay. Inclusion of 30-500 microM zinc in the exposure solution produced a zinc concentration-dependent, noncompetitive attenuation of NMDA-induced neuronal injury, with an ED50 of about 80 microM. In contrast, zinc produced the same concentration-dependent potentiation of quisqualate neurotoxicity; and with 500 microM zinc, a small potentiation of kainate neurotoxicity was suggested. The effect of zinc on the neurotoxicity of the broad-spectrum agonist glutamate was consistent with these effects on specific agonists, as well as with a previous study showing that glutamate neurotoxicity normally depends predominantly on NMDA-receptor activation. Zinc produced a concentration-dependent reduction in glutamate-induced neuronal injury in a fashion similar to that seen with NMDA, but less effectively. In addition, despite this overall protective effect, zinc paradoxically increased the glutamate-induced destruction of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d)-containing neurons, a subpopulation that was shown in the preceding paper (Koh and Choi, 1988) to exhibit resistance to NMDA receptor-mediated neurotoxicity, and vulnerability to non-NMDA receptor-mediated neurotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Zinc alters excitatory amino acid neurotoxicity on cortical neurons. 338 93

Interactive combinations of altered zinc and thyroid states were studied in rats to assess pathophysiologic effects. Clinical signs of zinc deficiency or thyroid alteration were limited to effects on growth rate. Changes in organ and glandular weights and serum thyrotropin levels reflected changes in serum thyroid hormone concentrations. Significantly (probability less than .001), zinc-deficient rats had enhanced hepatic thyroxine-5'-monodeiodinase activity. In addition, the zinc-deficient state was found to be protective against thiouracil-induced suppression of the microsomal-monooxygenase and thyroxine-5'-monodeiodinase enzyme complex. This protective effect was evident by greater thyroxine-5'-monodeiodinase and reduced nicotinamide-adenine dinucleotide phosphate cytochrome c reductase activities, as well as cytochrome P-450 content, in zinc-deficient/thiouracil-treated animals. Thus, the enzyme complex had increased triiodothyronine-generating capacity in conditions of zinc deficiency, which may be important because of the greater biological reactivity of triiodothyronine. Primary zinc deficiency conditions of the magnitude seen in this study and in this-age rat did not appear to alter serum thyroid hormone levels or organ/glandular function. However, concurrent zinc deficiency and altered thyroid status did change thyroid hormone response and disposition, which may be important to populations at risk because of thyroid dysfunctional states.
...
PMID:Effects of zinc deficiency on thyroid function. 360 29

The aim of this study was to describe the architecture of a ganglionated nerve plexus found in the loose connective tissue surrounding the pulmonary vein of the mouse. The input to this plexus was from the vagus nerves and from the stellate ganglia. A large ganglion containing more than 200 neurons was commonly found near the primary bifurcation of the pulmonary vein. The neurons were studied by NADH-diaphorase, zinc iodide-osmium and glyoxylic acid-induced catecholamine fluorescence methods at the light microscopic level, by scanning electron microscopy after the removal of connective tissue, and by transmission electron microscopy. The shape of the neuronal cell bodies was generally a smooth ellipsoid with the average major axis about twice the minor axis. The measured maximum cell diameter ranged from 14 to 42 micron (mean 26 micron). The profile area of individual neurons, as measured from wholemount preparations, ranged from 100 to 800 micron2 (mean 340 micron2) and the calculated neuronal volume ranged from 500 to 12,000 micron3 (mean 3300 micron3). Although there was this wide spread in neuronal size, histograms of cell size showed no separate populations of neurons. Almost all of the ganglionic neuronal cell bodies showed no catecholamine-specific fluorescence, but about 1% of the neurons exhibited a weak green fluorescence. Only a few noradrenergic nerve fibres were seen within the ganglia and these were associated with intraganglionic blood vessels. Small, intensely fluorescent cells were only rarely associated with the ganglia. Neurons and satellite cells formed units which were surrounded by an intraganglionic connective tissue space and a perineurium. Some of the intraganglionic capillaries were fenestrated. Neurons were entirely surrounded by satellite cells and did not appear to have any long dendrites. The generally smooth neuronal cell bodies had short spine-like processes, which were confined to within the satellite cell sheath. Preganglionic nerve fibres formed pericellular baskets of varicose fibres around neurons and made synapses either directly on the cell body or on somatic spines in about equal numbers. No synapses were found in the neuropil at a distance from the neuronal cell body. A few nerve processes were deeply embedded within the neuronal cell body. Clusters of vesicles were found in the cytoplasm of most neurons and were associated with subplasmalemmal densities. These synapse-like structures were mostly directed towards satellite cells, but some were associated with incoming synapses.
...
PMID:Fine structure of the autonomic ganglia of the mouse pulmonary vein. 362 38

Experiments were conducted to examine the role of zinc in the prevention of bromobenzene hepatoxicity in male rats. Bromobenzene (BB) (7.5 mmol/kg, ip) produced a marked hepatotoxicity as evidenced by increases in plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and a marked depression in hepatic glutathione (GSH) content 24 hr after administration. The administration of zinc (92 mumol Zn/kg, ip, at 48 and 24 hr prior to the bromobenzene) ameliorated the bromobenzene elevations in plasma AST (25%) and plasma ALT (50%) but did not alter the decreases in hepatic GSH. Following administration of [14C]BB, the radioactive label was distributed primarily in the cytosolic and lipid fractions derived from liver homogenates. Furthermore, the subcellular distribution of [14C]BB was not altered by zinc pretreatment. The extent of covalent binding of [14C]BB metabolites to hepatic tissue was significantly depressed in zinc-treated rats. Zinc induced the hepatic levels of metallothionein but [14C]BB did not bind to this sulfhydryl rich protein. Further experiments showed that zinc treatment depressed cytochrome P-450 content, the activity of NADPH cytochrome c reductase, and the metabolism of aniline, but not that of ethylmorphine. These studies suggest that the hepatoprotective effect of zinc against bromobenzene toxicity does not involve altered binding of the reactive toxic metabolite to glutathione or metallothionein, but it may be mediated by the inhibitory effect of zinc on the microsomal cytochrome P-450-dependent drug metabolizing system.
...
PMID:Amelioration of bromobenzene hepatotoxicity in the male rat by zinc. 398

Zinc content of testes, bones, esophagus, kidneys, and muscles was decreased, whereas iron content was increased in the testes of zinc-deficient rats compared to restrictedly fed control rats. Histochemical enzyme determinations revealed reduced activities of certain enzymes in the testes, bones, esophagus, and kidneys. In the testes, lactic dehydrogenase (LDH), malic dehydrogenase (MDH), alcohol dehydrogenase (ADH), and NADH diaphorase; in the bones, LDH, MDH, ADH, and alkaline phosphatase; in the esophagus, MDH, ADH, and NADH diaphorase; and in the kidneys, MDH and alkaline phosphatase were decreased in zinc-deficient rats compared to restrictedly fed controls. Succinic dehydrogenase (SDH) revealed no significant changes under the conditions of our experiments in various groups of rats that were investigated. In a "repleted" group of rats, content of zinc in testes and bones increased significantly, compared to the deficient group. The iron content of the testes decreased after repletion with zinc. In the testes, bones, esophagus, and kidneys, the activities of various enzymes increased after repletion with zinc. Inasmuch as the major manifestations of zinc deficiency syndrome in the rat include growth retardation, testicular atrophy, and esophageal parakeratosis, our results suggest that the content of zinc in the above tissues most likely controls the physiological processes through the formation of zinc-dependent enzymes.
...
PMID:Studies on zinc deficiency: changes in trace elements and enzyme activities in tissues of zinc-deficient rats. 429 21

We have found neural nitric oxide synthase (nNOS) activity to be completely and reversibly inhibited by Zn2+ ion with an apparent Ki of 30 microM. Zn2+ blocks NADPH-dependent reduction of heme iron in nNOS and also blocks the calmodulin-dependent superoxide-mediated cytochrome c reductase activity exhibited by nNOS. However, Zn2+ ion has no apparent effect on the calmodulin-independent direct reduction of cytochrome c by nNOS. Zn2+ ion induces perturbation difference spectra in nNOS characterized by the appearance of a peak at approximately 430 nm and a trough at approximately 395 nm, with an apparent spectral binding constant of 50 microM. These spectral changes are consistent with a Zn(2+)-dependent change in the spin-state equilibrium of the heme iron in nNOS. The spectral binding constant for L-arginine binding to nNOS (approximately 1.5 microM) is not significantly affected by the presence of 50 microM Zn2+, indicating that Zn(2+)-dependent inhibition of nNOS activity is not due to interference with substrate binding. The estimated maximal change in nNOS absorbance at approximately 418 nm caused by the L-arginine-dependent conversion of the ferric heme iron from hexacoordinate low-spin to pentacoordinate high-spin is increased by 50% in the presence of 50 microM Zn2+, which reflects the increased initial amount of low-spin ferric heme iron present. These data indicate that Zn(2+)-dependent inhibition of nNOS activity is due to binding of Zn2+ to the hemoprotein domain in the enzyme and that inhibition is associated with perturbations in the environment of the heme iron that appear to block its ability to mediate oxygen reduction.
...
PMID:Inhibition of nitric oxide synthase activity by Zn2+ ion. 757 22


1 2 3 Next >>

---