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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cadmium nitrate, acetate and sulphate cause death of root meristems of Allium sativum at 5.10(-7) Mol/ml concentration for the two first ones and 10(-7) Mol/ml for the last one. Lower concentrations do not induce chromosomal aberrations. As to the cellular toxicity, cadmium salts are between phenyl-mercuric-hydroxid and lead nitrate, the first one being the most active.
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PMID:[Cytotoxicity of cadmium : study on root meristems of Allium sativum L]. 14 Jul 26

The effects of erythromycin, chloramphenicol, cycloheximide, pyrimethamine, chromate, cadmium, lead, nickel, 4-nitro-quinoline-1-oxide and thioacetamide on yeast and human cells were studied. Inhibition of the synthesis of mitochondrial proteins resulted in the loss of cytochromes as well as in morphological changes in the cellular membranes and mitotic arrest. The data are discussed.
Mol Cell Biochem 1977 Feb 04
PMID:Mitochondrial biogenesis: inhibitors of mitochondrial protein synthesis. 40 20

1. Chromatography measurements indicated that adult rats converted 25-hydroxycholecalciferol into 1,25-dihydroxycholecalciferol at a lower rate than that reported earlier for young animals. In serum, less-polar metabolites were found which probably represented vitamin D esters and vitamin D3. 2. A low dietary intake of calcium resulted in an evident increase in the fraction corresponding to 1,25-dihydroxycholecalciferol in the kidneys and also in the intestinal mucosa and serum. 3. Inclusion of 0.67 mmol of cadmium/l of drinking water at a low dietary intake of calcium resulted in an increased accumulation of both cadmium and zinc in the kidneys and liver compared with values at a normal dietary calcium intake. 4. At a normal dietary calcium intake, cadmium exposure caused inhibited production of 1,25-dihydroxycholecalciferol by the kidneys and an increased accumulation of 24,25-dihydroxycholecalciferol, vitamin D3 and vitamin D esters in the serum. 5. The inhibitory effect of cadmium on the renal conversion of 25-hydroxycholecalciferol into 1,25-dihydroxycholecalciferol was almost completely counteracted by a simultaneous low dietary calcium intake. Cadmium-exposed, calcium-deficient animals also showed a maintained accumulation of 1,25-dihydroxycholecalciferol in the intestinal mucosa.
Clin Sci Mol Med 1977 Nov
PMID:Vitamin D metabolism in adult rats at low and normal calcium intake and the effect of cadmium exposure. 58 28

1. Nine-months-old male rats were divided into a normal control group and one experimental group which received eight daily intraperitoneal injections 15 pmol of 1,25-dihydroxycholecalciferol/100 g body weight. After 5 days, 20 muCi of 109CdCl2 or 20muCi of 45CaCl2 was administered by stomach tube. The intestinal absorption and tissue retention of the radioisotopes were analysed during the next 3 days, the animals being kept in metabolic cages. 2. The administration of 1,25-dihydroxycholecalciferol caused significantly increased net absorption of intestinal calcium, hypercalcaemia and increased incorporation of calcium into bone. In comparison, there was no significant effect on the intestinal absorption of trace doses of cadmium or upon the accumulation of cadmium in the liver and kidneys.
Clin Sci Mol Med 1978 Aug
PMID:Intestinal absorption and tissue retention of cadmium and calcium in normal adult rats and rats given an active metabolite of vitamin D (1,25-dihydroxycholecalciferol). 67 27

Studies on the circular dichroic spectrum of cobalt-substituted concanavalin A have been continued in particular with respect to calcium- and saccharide-induced spectral pertubations reported previously (Kalb, A.J. and Pecht, I. (1973) Biochim. Biophys. Acta 303, 264-268; Richardson, C.E. and Behnke, W.D. (1976) J. Mol. Biol. 102, 441-451). We find that the addition of calcium or cadmium to (CO2+)-concanavalin A induces slow time-dependent alterations in the extrinsic cotton effects. Moreover, one equivalent of calcium is sufficient to cause maximal changes in the cobalt spectrum provided sufficient time is allowed for the effect to be observed. The addition of mono, di-and trisaccharides, specific for concanavalin A, have no resolvable effect upon the cobalt spectrum of concanavalin A (Richardson, C.E. and Behnke, W.D. (1976) J. Mol. Biol. 102, 441-451). The data presented here suggest that these time-dependent processes are conformationally mediated and occur subsequent to S2 occupancy. Evidence is presented that a particular calcium-cobalt-concanavalin A conformer exists which is responsible for the generation of activity in a light-scattering assay system.
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PMID:Cobalt-concanavalin A. An index of inactive and active conformational states. 72 53

1. Plasma cadmium and zinc were determined by atomic absorption spectrophotometry in inferior venal caval or peripheral venous blood in thrity hypertensive patients and fifteen normal subjects. 2. The mean plasma cadium in hypertensive patients was significantly higher than in normal control subjects. 3. The plasma cadmium/zinc ratio was significantly greater in hypertensive patients. 4. There was a significant positive correlation between the plasma cadmium/zinc ratio and the mean arterial blood pressure.
Clin Sci Mol Med 1976 Nov
PMID:Plasma cadmium and zinc in human hypertension. 99 45

The ability of cations to modulate the binding of the sigma 1 receptor-selective ligand (+)-[3H]pentazocine to guinea pig cerebellum was investigated. Di- and trivalent cations biphasically inhibited (+)-[3H]pentazocine binding, revealing multiple affinity states. The rank order of potency of these cations (based on the high affinity component of inhibition) was Zn2+ > Co2+ >> La3+ = Ni2+ = Cd2+ = Mn2+ = Gd2+ > Ba2+ = Sr2+ >> Mg2+ > Ca2+. The inhibition of 1,3-[3H]di(2-tolyl)guanidine binding to the sigma 2 receptor by these cations differed qualitatively and quantitatively from their effects on (+)-[3H]pentazocine binding. Although monovalent cations decreased the Kd for (+)-[3H]pentazocine binding, divalent cations split (+)-[3H]pentazocine binding into low and high affinity components. The Bmax of the high affinity component decreased with increasing divalent cation concentrations. Both mono- and divalent cations significantly reduced the rate of association of (+)-[3H]pentazocine with the sigma 1 receptor without altering the dissociation rate. (+)-[3H]Pentazocine binding was not altered by guanine nucleotides or by treatment with cholera or pertussis toxins. However, nonselective cation channel blockers (cinnarizine, hydroxyzine, prenylamine, amiodarone, and proadifen) potently inhibited (+)-[3H]pentazocine binding. These results indicate that physiologically relevant concentrations of divalent cations allosterically modulate (+)-[3H]pentazocine binding to the sigma 1 receptor, to reveal multiple affinity states. These sites do not represent sigma 1 to sigma 2 subtype interconversion or ternary complex formation with guanine nucleotide-binding proteins. However, the rank order of cation potency and the inhibition of binding by cation channel blockers is consistent with a potential role for sigma receptors as constituents of cation channels.
Mol Pharmacol 1992 Nov
PMID:Modulation of (+)-[3H]pentazocine binding to guinea pig cerebellum by divalent cations. 127 78

The effect of regucalcin, a calcium-binding protein isolated from rat liver cytosol, on deoxyuridine 5'-triphosphatase (dUTPase) in the cytosol of rat liver was investigated. Addition of Ca2+ up to 5.0 microM to the enzyme reaction mixture caused a significant decrease of dUTPase activity, while Zn2+, Cd2+, Co2+, Al3+, Mn2+ and Ni2+ (10 microM) did not have an appreciable effect. The Ca(2+)-induced decrease of dUTPase activity was reversed by the presence of regucalcin; the effect was complete at 1.0 microM of the protein. Regucalcin had no effect on the basal activity of the enzyme. Meanwhile, the reversible effect of regucalcin on the Ca2+ (10 microM)-induced decrease of dUTPase activity was not altered by the coexistence of Cd2+ or Zn2+ (10 microM). The present data suggest that liver cytosolic dUTPase is uniquely regulated by Ca2+ of various metals, and that the Ca2+ effect is reversed by regucalcin.
Mol Cell Biochem 1992 Mar 04
PMID:Reversible effect of calcium-binding protein regucalcin on the Ca(2+)-induced inhibition of deoxyuridine 5'-triphosphatase activity in rat liver cytosol. 131 24

The backbone dynamics of the EF-hand Ca(2+)-binding protein, calbindin D9k, has been investigated in the apo, (Cd2+)1 and (Ca2+)2 states by measuring the rate constants for amide proton exchange with solvent. 15N-1H correlation spectroscopy was utilized to follow direct 1H-->2H exchange of the slowly exchanging amide protons and to follow indirect proton exchange via saturation transfer from water to the rapidly exchanging amide protons. Plots of experimental rate constants versus intrinsic rate constants have been analyzed to give qualitative insight into the opening modes of the protein that lead to exchange. These results have been interpreted within the context of a progressive unfolding model, wherein hydrophobic interactions and metal chelation serve to anchor portions of the protein, thereby damping fluctuations and retarding amide proton exchange. The addition of Ca2+ or Cd2+ was found to retard the exchange of many amide protons observed to be in hydrogen-bonding environments in the crystal structure of the (Ca2+)2 state, but not of those amide protons that were not involved in hydrogen bonds. The largest changes in rate constant occur for residues in the ion-binding loops, with substantial effects also found for the adjacent residues in helices I, II and III, but not helix IV. The results are consistent with a reorganization of the hydrogen-bonding networks in the metal ion-binding loops, accompanied by a change in the conformation of helix IV, as metal ions are chelated. Further analysis of the results obtained for the three states of metal occupancy provides insight into the nature of the changes in conformational fluctuations induced by ion binding.
J Mol Biol 1992 Oct 20
PMID:Nuclear magnetic resonance studies of the internal dynamics in Apo, (Cd2+)1 and (Ca2+)2 calbindin D9k. The rates of amide proton exchange with solvent. 133 70

The rat thyrotropin-releasing hormone (TRH) precursor (prepro-TRH) contains five copies of the TRH progenitor sequence linked together by intervening sequences. Recently, we have shown that the connecting peptides prepro-TRH-(160-169) (Ps4) and prepro-TRH-(178-199) (Ps5) are released from rat hypothalamic neurones in response to elevated potassium concentrations, in a calcium-dependent manner. In the present study, the role of voltage-operated calcium channels in potassium-induced release of Ps4 and Ps5 was investigated, using a perifusion system for rat hypothalamic slices. The release of Ps4 and Ps5 stimulated by potassium (70 mM) was blocked by the inorganic ions Co2+ (2.6 mM) and Ni2+ (5 mM). In contrast, the stimulatory effect of KCl was insensitive to Cd2+ (100 microM). The dihydropyridine antagonist nifedipine (10 microM) had no effect on K(+)-evoked release of Ps4 and Ps5. Furthermore, the response to KCl was not affected by nifedipine (10 microM) in combination with diltiazem (1 microM), a benzothiazepine which increases the affinity of dihydropyridine antagonists for their receptor. The dihydropyridine agonist BAY K 8644, at concentrations as high as 1 mM, did not stimulate the basal secretion of Ps4 and Ps5. In addition, BAY K 8644 had no potentiating effect on K(+)-induced release of Ps4 and Ps5. The marine cone snail toxin omega-conotoxin, a blocker of both L- and N-type calcium channels had no effect on the release of Ps4 and Ps5 stimulated by potassium. Similarly, the omega-conopeptide SNX-111, a selective blocker of N-type calcium channels, did not inhibit the stimulatory effect of potassium. The release of Ps4 and Ps5 evoked by high K+ was insensitive to the non-selective calcium channel blocker verapamil (20 microM). Amiloride (1 microM), a putative blocker of T-type calcium channels, did not affect KCl-induced secretion of the two connecting peptides. Taken together, these results indicate that two connecting peptides derived from the pro-TRH, Ps4 and Ps5, are released by K(+)-induced depolarization through activation of voltage-sensitive calcium channels. The calcium channels appear to have a pharmacological profile different from that of L- and N-type channels. Although, their insensitivity to low Cd2+ concentrations and sensitivity to Ni2+ ions would support the involvement of T-type calcium channels, the lack of effect of amiloride suggests that they belong to a yet undefined class of calcium channels.
Brain Res Mol Brain Res 1992 Jul
PMID:Omega-conotoxin- and nifedipine-insensitive voltage-operated calcium channels mediate K(+)-induced release of pro-thyrotropin-releasing hormone-connecting peptides Ps4 and Ps5 from perifused rat hypothalamic slices. 133 51


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