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1.
Gizatullina ZZ Gaynutdinov TM Svoboda H Jerzembek D Knabe A Vielhaber S Malesevic M Heinze HJ Fischer G Striggow F Gellerich FN 《Mitochondrion》2011,11(3):421-429
We studied the functional properties of isolated brain mitochondria (BM) prepared from total rat brain (BM(total)) or from cerebral subregions under basal and Ca(2+) overload conditions in order to evaluate the effects of cyclosporine A (CsA) in a regiospecific manner. CsA-induced effects were compared with those of two derivatives-the none-immunosuppressive [O-(NH(2)(CH2)(5)NHC(O)CH(2))-D-Ser](8)-CsA (Cs9) and its congener, the immunosuppressive [D-Ser](8)-CsA. The glutamate/malate-dependent state 3 respiration of mitochondria (state 3(glu/mal)) differed in region-specific manner (cortex > striatum = cerebellum > substantia nigra > hippocampus), but was significantly increased by 1μM CsA (+21±5%) in all regions. Ca(2+) overload induced by addition of 20μM Ca(2+) caused a significant decrease of state 3(glu/mal) (-45 to -55%) which was almost completely prevented in the presence of 1μM CsA, 1μM Cs9 or 1μM [D-Ser](8)-CsA. Mitochondrial Ca(2+) accumulation thresholds linked to permeability transition (PT) as well as the rate and completeness of mitochondrial Ca(2+) accumulation differed between different brain regions. For the first time, we provide a detailed, regiospecific analysis of Ca(2+)-dependent properties of brain mitochondria. Regardless of their immunosuppressive impact, CsA and its analogues improved mitochondrial functional properties under control conditions. They also preserved brain mitochondria against Ca(2+) overload-mediated PT and functional impairments. Since Cs9 does not mediate immunosuppression, it might be used as a more specific PT inhibitor than CsA. 相似文献
2.
Cyclosporin A (CsA) nonimmunosuppressive analogs were evaluated against Trypanosoma cruzi and on TcCyP19, a cyclophilin of 19 kDa. Two out of eight CsA analogs, H-7-94 and F-7-62 showed the best anti-parasitic effects on all in vitro assays. Their IC(50) values were 0.82 and 3.41 microM, respectively, compared to CsA IC(50) value 5.39 microM on epimastigote proliferation; and on trypomastigote lysis their IC(50) values were 0.97 and 2.66 microM compared to CsA IC(50) value 7.19 microM. H-7-94 and F-7-62 were also more effective than CsA in inhibiting trypomastigote infection. The enzymatic activity of TcCyP19 was inhibited by all CsA derivatives, suggesting this target is involved in the trypanocidal effects observed. 相似文献
3.
R Cirillo M Triggiani L Siri A Ciccarelli G R Pettit M Condorelli G Marone 《Journal of immunology (Baltimore, Md. : 1950)》1990,144(10):3891-3897
We have examined the effects of cyclosporin A (CsA) and a series of CsA analogs that bind with decreasing affinity to cyclophilin, to evaluate the involvement of this protein in the release of preformed (histamine) and de novo synthesized (peptide leukotriene C4; LTC4) mediators of inflammatory reactions from human basophils. CsA (8 to 800 nM) concentration-dependently inhibited (5 to 60%) histamine release from peripheral blood basophils challenged with anti-IgE. CsA was more potent (92.6 +/- 1.8 vs 59.1 +/- 4.5%; p less than 0.001) and, at low concentrations, more effective when the channel-operated influx of Ca2+ was bypassed by the ionophore A23187 (IC40 = 24.1 +/- 3.9 vs 105.5 +/- 22.2 nM; p less than 0.05). CsA had no effect on the release of histamine caused by phorbol myristate and bryostatin 1 that activate different isoforms of protein kinase C. Inhibition of histamine release from basophils challenged with anti-IgE was not abolished by washing (three times) the cells before anti-IgE challenge. CsA also inhibited the de novo synthesis of LTC4 from basophils challenged with anti-IgE. The inhibitory effect of CsA was very rapid, and the drug, added from 1 to 10 min during the reaction, inhibited the ongoing release of histamine caused by anti-IgE and by A23187. The experiments with CsA analogs (CsG, CsC, CsD, and CsH) showed that CsH, which has an extremely low affinity for cyclophilin, has no effect on basophil mediator release. In addition, there is a significant correlation between the concentrations of CsA, G, C, and D that inhibited by 30% the histamine release induced by anti-IgE (r = 0.99; p less than 0.001) and by A23187 (r = 0.87; p less than 0.001) and their affinity for cyclophilin. 相似文献
4.
Sonata Trumbeckaite Zemfira Gizatullina Odeta Arandarcikaite Peter Röhnert Stefan Vielhaber Miroslav Malesevic Gunter Fischer Enn Seppet Frank Striggow Frank Norbert Gellerich 《Mitochondrion》2013,13(5):539-547
We have introduced a sensitive method for studying oxygen/glucose deprivation (OGD)-induced mitochondrial alterations in homogenates of organotypic hippocampal slice cultures (slices) by high-resolution respirometry. Using this approach, we tested the neuroprotective potential of the novel non-immunosuppressive cyclosporin (CsA) derivative Cs9 in comparison with CsA, the immunosuppressive CsA analog [D-Ser]8CsA, and MK 801, a N-methyl-d-aspartate (NMDA) receptor antagonist. OGD/reperfusion reduced the glutamate/malate dependent (and protein-related) state 3 respiration to 30% of its value under control conditions. All of the above drugs reversed this effect, with an increase to > 88% of the value for control slices not exposed to OGD. We conclude that Cs9, [D-Ser]8CsA, and MK 801, despite their different modes of action, protect mitochondria from OGD-induced damage. 相似文献
5.
A mutation in alpha helix 3 of CA renders human immunodeficiency virus type 1 cyclosporin A resistant and dependent: rescue by a second-site substitution in a distal region of CA
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The replication of many isolates of human immunodeficiency virus type 1 (HIV-1) is enhanced by binding of the host cell protein cyclophilin A (CypA) to the viral capsid protein (CA). The immunosuppressive drug cyclosporine A (CsA) and its nonimmunosuppressive analogs bind with high affinity to CypA and inhibit HIV-1 replication. Previous studies have identified two mutations, A92E and G94D, in the CypA-binding loop of CA that confer the ability of HIV-1 to replicate in the presence of CsA. Interestingly, CsA stimulates the replication of HIV-1 mutants containing either the A92E or G94D substitution in some human cell lines. Here, we show that substitution of alanine for threonine at position 54 of CA (T54A) also confers HIV-1 resistance to and dependence on CsA. Like the previously identified CsA-resistant/dependent mutants, infection by the T54A mutant was stimulated by CsA in a target cell-specific manner. RNA interference-mediated reduction of CypA expression enhanced the permissiveness of HeLa cells to infection by the T54A mutant. A suppressor mutation, encoding a substitution of threonine for alanine at position 105 of CA (A105T), was identified through adaptation of the T54A mutant virus for growth in CEM cells. A105T rescued the impaired single-cycle infectivity and replication defects of both T54A and A92E mutants. These results indicate that CA determinants outside the CypA-binding loop can modulate the dependence of HIV-1 infection on CypA. 相似文献
6.
M Demeule A Laplante A Sepehr-Araé E Beaulieu D Averill-Bates R M Wenger R Béliveau 《Biochimie et biologie cellulaire》1999,77(1):47-58
The interaction between P-glycoprotein (P-gp) from membranes isolated from multidrug-resistant Chinese hamster ovary cells and cyclosporin A (CsA) analogues and its metabolites was characterized. Screening of these latter as chemosensitizers was performed using three different assays: (i) vinblastine uptake, (ii) photoaffinity labeling by [125I]iodoaryl azidoprazosin, and (iii) P-gp ATPase activity. Oxidation of the hydroxyl group at position I of CsA (200-096), CsG (215-834), or CsD (PSC-833) increased their inhibition of P-gp. CsA analogues (208-032, 208-183) modified at position 11 retained their ability to inhibit P-gp while analogues modified at position 2 (CsC and CsD) lost their efficiency. The inhibitions induced by metabolites of CsA were also compared to those obtained with CsG metabolites. From all the molecules tested, PSC-833 and 280-446 peptolide were the strongest inhibitors. Our results indicate that modifications of CsA analogues at position 1 and 2 are critical for their interaction with P-gp and that CsA metabolites retain a portion of the inhibitory activity of the parent drug. 相似文献
7.
Schistosoma japonicum is less sensitive to cyclosporin A in vivo than Schistosoma mansoni. 总被引:1,自引:0,他引:1
We compared the toxic effects of cyclosporin A (CsA) on postmigratory immature Schistosoma mansoni and Schistosoma japonicum in mice. For each species, CsA was administered either relatively early or late during development. Exposure of 20-day-old S. mansoni to 1 subcutaneous dose of CsA (50 mg/kg) reduced the worm burden by 45% and induced herniae and/or boli of the gut in 32% of perfusable worms. These results agree with previous reports. In addition, CsA induced a marked liver shift (37% of total worm number). For S. japonicum, CsA was administered at 11 days postinfection (PI) because this species migrates more quickly. Killing of worms and damage to the gut were not observed, and only a slight liver shift occurred. Similarly, these effects were not recorded when CsA was administered at the later times of 34 days PI for S. mansoni and 17 days PI for S. japonicum. For both species, CsA stunted worms, affecting both sexes early PI but only females late PI. In conclusion, immature worms of S. japonicum are less sensitive than S. mansoni to CsA. Also, S. mansoni displays marked age-dependent differences in its sensitivity to CsA. 相似文献
8.
P R Gooley P L Durette J Boger I M Armitage 《International journal of peptide and protein research》1991,37(5):351-363
MeAla6-cyclosporin A (MeAla6-CsA) is a unique CsA analog that shows weak immunosuppressive activity and yet binds strongly to the proposed cytosolic protein receptor, cyclophilin (CyP). Preliminary 1H NMR data showed significant chemical shift differences between spectra of MeAla6-CsA and CsA, suggesting different preferred conformations. A more detailed study, however, revealed that the backbone conformations of the two molecules are essentially identical, and that the differences can be accounted for, principally, by the sidechain motions of the MeBmt-1, MeLeu-9, and -10 residues. ROE and coupling constant data show that in MeAla6-CsA, the preferred chi 1 rotamers for MeLeu-9 and -10 are + 180 degrees (T), whereas in CsA there is a more even distribution of rotamer populations for MeLeu-10, and a preferred -60 degrees (G-) chi 1 rotamer for MeLeu-9. Similar data argue that the sidechain of MeBmt-1 is more restricted in its motion in MeAla-CsA than in CsA. Temperature studies suggest that these preferred rotamers for MeAla6-CsA may increase the stability of the hydrogen bond between NH(7) and CO(11), but prevent particular residues, especially the essential MeBmt-1 sidechain, from adopting orientations required to elicit immunosuppressive activity. The significant changes observed in the preferred orientations for the sidechains of the MeBmt-1, MeLeu-9, and MeLeu-10 residues in MeAla6-CsA argue that the particular orientations which they assume in CsA are not essential for cyclophilin binding. 相似文献
9.
K Wenzel-Seifert L Grünbaum R Seifert 《Journal of immunology (Baltimore, Md. : 1950)》1991,147(6):1940-1946
Cyclosporin (Cs)A but not CsH inhibits activation of human lymphocytes. We studied the effects of CsA, CsD, and CsH on human neutrophil activation induced by chemoattractants and by various substances that circumvent receptor stimulation. CsH inhibited superoxide (O2-) formation induced by the chemotactic peptide, FMLP (30 nM), with a half-maximal effect at 40 nM. O2- formation was abolished by CsH at 1 microM. CsH increased the concentration of FMLP causing half-maximal activation of O2- formation from 30 nM to 0.8 microM and substantially reduced the stimulatory effect of FMLP at supra-maximally effective concentrations. The inhibitory effect of CsH on O2- formation was evident immediately after addition to neutrophils. CsH also markedly inhibited the increase in cytosolic Ca2+ ([Ca2+]i), beta-glucuronidase, and lysozyme release and aggregation stimulated by FMLP. CsA and CsD were considerably less effective than CsH to inhibit FMLP-induced O2- formation. CsA and CsD were without effect on exocytosis, rises in [Ca2+]i, and aggregation induced by the chemotactic peptide. Cyclosporines inhibited FMLP-induced O2- formation in an additive manner, indicating that they acted through a mechanism they had in common. Cyclosporines only slightly inhibited O2- formation and lysozyme release induced by C5a. Aggregation and rises in [Ca2+]i stimulated by C5a were not affected by cyclosporines, and they did not inhibit O2- formation and exocytosis induced by platelet-activating factor and leukotriene B4. Cyclosporines partially inhibited O2- formations induced by NaF and gamma-hexachlorocyclohexane. CsA marginally inhibited PMA-induced O2- formation and lysozyme release. CsA, CsD, and CsH did not inhibit arachidonic acid-induced O2- formation and its potentiation by NaF or stable guanine nucleotides in a cell-free system from DMSO-differentiated HL-60 cells. CsH partially inhibited binding of FML [3H]P to formyl peptide receptors in membranes from DMSO- or dibutyryl cAMP-differentiated HL-60 cells. Our data show that: 1) cyclosporines differentially inhibit activation of human neutrophils; and 2) CsH is, indeed, not immunologically inactive but is a potent and effective inhibitor of FMLP-induced O2- formation. 3) CsH interferes with agonist binding to formyl peptide receptors and in addition, cyclosporines may also act at sites distal to chemoattractant receptors. 相似文献
10.
Cyclosporin A (CsA) is a cyclic endecapeptide of fungal origin displaying strong immunosuppressive properties. CsA and another active member of the cyclosporin (Cs) family, but not an inactive one, can interfere with the proliferation of some, but not all, T-lymphoid cell lines. Cells from Cs-sensitive lines accumulate in the G1 phase of the cell cycle. No effect is detected on the cycle of Cs-resistant lines. Both Cs-sensitive and Cs-resistant lines are arrested by another G1 blocker (actinomycin D) and DNA synthesis inhibitors (cytosine arabinoside, hydroxyurea), become multinucleated/polyploid when exposed to cytochalasin B (CB), are arrested in mitosis by colchicine and accumulate in G2 phase in the presence of Taxol. The effect of Cs is best evidenced when the drug is applied to cells which were already delayed in G1 by saturation density cultivation or serum deprivation. By the combined use of Cs and of other drugs working at a later phase of the cycle, results were obtained which suggest that the effect of Cs is either to delay very much the cells throughout the G1 phase or to arrest them at that G1 phase or at the following one. A correlation of the G1-blocking property of Cs with their immunosuppressive properties may be possible but is still speculative. 相似文献
11.
Evaluation of the anti-hepatitis C virus effects of cyclophilin inhibitors, cyclosporin A, and NIM811 总被引:3,自引:0,他引:3
Goto K Watashi K Murata T Hishiki T Hijikata M Shimotohno K 《Biochemical and biophysical research communications》2006,343(3):879-884
Hepatitis C virus (HCV) is a major causative agent of hepatocellular carcinoma. We recently discovered that the immunosuppressant cyclosporin A (CsA) and its analogue lacking immunosuppressive function, NIM811, strongly suppress the replication of HCV in cell culture. Inhibition of a cellular replication cofactor, cyclophilin (CyP) B, is critical for its anti-HCV effects. Here, we explored the potential use of CyP inhibitors for HCV treatment by analyzing the HCV replicon system. Treatment with CsA and NIM811 for 7 days reduced HCV RNA levels by 2-3 logs, and treatment for 3 weeks reduced HCV RNA to undetectable levels. NIM811 exerted higher anti-HCV activity than CsA at lower concentrations. Both CyP inhibitors rapidly reduced HCV RNA levels even further in combination with IFNalpha without modifying the IFNalpha signal transduction pathway. In conclusion, CyP inhibitors may provide a novel strategy for anti-HCV treatment. 相似文献
12.
The effects of several imidazole antimycotic agents, an imidazole and several mineralocorticoid analogs on the cytochrome P-450(11)beta-catalyzed 11 beta-hydroxylation of 11-deoxycorticosterone and aldosterone synthesis were examined. Ketoconazole, clotrimazole, miconazole and etomidate were found to be potent inhibitors of the reactions, causing 50% inhibition of the 11 beta-hydroxylase activity at concentrations between 10(-8) and 10(-7) M. The potency of etomidate as to the inhibition of aldosterone- and 18-hydroxycorticosterone-production was found to be almost equal to that in the case of 11 beta-hydroxylation. Spironolactone and other newly synthesized mineralocorticoid analogs were also found to inhibit the cytochrome P-450(11)beta-mediated reactions. The ID50 values of these drugs for inhibition of the 11 beta-hydroxylase activity were almost equal to those in the case of the aldosterone- and 18-hydroxycorticosterone-biosynthetic activities. The results of kinetical studies indicated that one of the mineralocorticoid analogs, Compound 23-0586, acts as a competitive inhibitor for the cytochrome P-450(11)beta-mediated reactions. 相似文献
13.
14.
[Glu34]-thymopoietin II fragment 32-45 and its three analogs were prepared by substitution of the amino acid residue at position 37. These peptides were synthesized by a conventional solution method, followed by deprotection with 1 M trifluoromethanesulfonic acid-thioanisole in trifluoroacetic acid in the presence of m-cresol. These peptides were tested for their effects on impaired T-cell transformation by phytohemagglutinin in the common variable immunodeficiency. The relative potency of the synthetic [Glu34]-thymopoietin II fragment 32-45 was one-half of that of synthetic thymopoietin II fragment 32-45. Among these tetradecapeptide analogs, one analog in which Val37 was replaced by Ile exhibited a potent activity which was more than that of the synthetic [Glu34]-thymopoietin II fragment 32-45. The relative potencies of Thr37 and Tyr37 analogs were one-third and one-half, respectively of that of the synthetic [Glu34]-thymopoietin II fragment 32-45. 相似文献
15.
Claus Spitzfaden Hans-Peter Weber Werner Braun Joerg Kallen Gerhard Wider Hans Widmer Malcolm D. Walkinshaw Kurt Wüthrich 《FEBS letters》1992,300(3):291-300
The previously determined 3D NMR solution structure of cyclophilin-bound cyclosporin A (CsA) was docked onto the X-ray crystal structure of cyclophilin. Intermolecular nuclear Overhauser effects (NOE) between CsA and cyclophilin were used as constraints in a restrained energy minimization to generate a model of the complex which satisfied all the NOE distance constraints. The model shows that the residues 9 to 11 and 1 to 5 of the cyclic CsA molecule are in contact with cyclophilin. Comparing the model of the CsA—cyclophilin complex to the X-ray crystal structure of a complex of cyclophilin with a substrate for peptidyl-proline cis-trans isomerase activity, i.e. the linear tetrapeptide substrate ae-Ala-Ala-Pro-Ala-amc (ac. acetyl; amc. amidomethylcoumarin), one notices that the contacting peptide segments in the two ligands are oriented in opposite directions, and that the side chain or MeVal-11 of CsA superposes rather precisely with the position of the prolyl residue in ae-Ala-Ala-Pro-Ala-amc. 相似文献
16.
A peptide based on the complementarity determining region (CDR) 3 of a pathogenic anti-DNA 16/6 Id(+) monoclonal antibody was previously shown to be a dominant T-cell epitope in experimental SLE, and to be capable of inhibiting SLE-associated proliferative responses. Single amino acid-substituted analogs of pCDR3 were designed and analyzed for their ability to stimulate or inhibit the proliferation of a pCDR3-specific T-cell line. Alterations in positions 9 and 10 neutralized the proliferative potential of pCDR3, whereas alterations in positions 6-8 and 11-15 retained the proliferative potential of the peptides. Similar to pCDR3, its analogs Ala11 and Nle13 inhibited efficiently the in vivo priming of lymph node cells either to pCDR3 or to the human monoclonal anti-DNA 16/6 Id(+) antibody. Substituting both positions 11 (Tyr --> Ala) and 13 (Met --> Nle) reduced this inhibitory capacity compared to the single substituted analogs. Also, truncation of pCDR3 at the C- and/or N-terminus obliterated the inhibitory activities of the peptide. Analogs Ala11 and Nle13 immunomodulated serological and clinical smanifestations of experimental SLE. Nevertheless, the original pCDR3 was a more efficient modulator of the disease. 相似文献
17.
B Xue R M Dersarkissian R L Baer G J Thorbecke D V Belsito 《Journal of immunology (Baltimore, Md. : 1950)》1986,136(11):4128-4133
Cyclosporin A (CsA) treatment of mice during the first 4 days of the sensitization phase prevents induction of contact sensitivity to trinitrochlorobenzene (TNCB). Administration of CsA on the day of ear challenge with TNCB also inhibits the effector phase of this response. Simultaneous treatment of the mice with IL 2-containing murine lymphokine preparations or with recombinant human IL 2 reverses the effect of CsA on the induction of contact sensitivity. Recombinant IL 2 also reverses the inhibition by CsA of the effector phase. Neither phase of the response is restored by murine IFN-gamma. Anti-body production to trinitrophenylated (TNP) Ficoll or TNP-hemocyanin is also strongly inhibited (greater than 75%) by CsA injected on the day of antigen injection. Although lymphokines or endotoxin may strongly enhance these responses, no reversal of the effect of CsA can be obtained. We conclude that inhibition of IL 2 production is of paramount importance for the inhibitory effect of CsA on contact sensitivity, but that additional effects are involved in the inhibition of antibody production to both T-dependent and T-independent antigens. 相似文献
18.
Prolactin receptors on human T and B lymphocytes: antagonism of prolactin binding by cyclosporine 总被引:13,自引:0,他引:13
D H Russell R Kibler L Matrisian D F Larson B Poulos B E Magun 《Journal of immunology (Baltimore, Md. : 1950)》1985,134(5):3027-3031
Prolactin (PRL) receptors have been identified recently on human peripheral blood mononuclear cells (MNC) and may be involved in the regulation of cell-mediated immunity. Cyclosporine (CsA), an immunosuppressive cyclic endecapeptide utilized to prolong graft survival in human organ transplant patients, affects PRL binding to MNC. At concentrations of CsA from 10(-10) through 10(-8) M, the amount of PRL bound to MNC markedly increased to ca. 400% of controls, whereas CsA concentrations of 10(-6) and 10(-5) M totally inhibited PRL binding to lymphocytes. The ability of low concentrations of CsA to enhance PRL binding was temperature-dependent and did not occur when binding assays were conducted at 4 degrees C. PRL displaced [3H]CsA from lymphocytes with ca. 50% displacement at 10(-9) M PRL and total displacement at concentrations of 10(-7), 10(-6), and 10(-5) M. Growth hormone did not displace [3H]CsA in similar experiments. CsA also did not alter the binding of a beta-receptor antagonist to MNC, again suggesting that CsA was specific in its antagonism of PRL binding. A CsA analog with no immunosuppressive action, cyclosporin H, did not alter PRL binding to MNC. Furthermore, PRL receptors were demonstrated on four cell lines of human and mouse origin. Finally, PRL receptors were identified on purified populations of T and B lymphocytes isolated from human spleens, and CsA again inhibited PRL binding at concentrations of 10(-7) and 10(-6) M. The presence of PRL receptors on T and B lymphocytes suggests that PRL may be involved in the regulation of humoral and cell-mediated immunity, and that one effect of CsA on immune function may be its ability to inhibit the effects of PRL action on these lymphocytes. 相似文献
19.
Wang JQ Pollok KE Cai S Stantz KM Hutchins GD Zheng QH 《Bioorganic & medicinal chemistry letters》2006,16(2):331-337
New carbon-11 labeled D-luciferin analogs D-luciferin [(11)C]methyl ester ([(11)C]LMEster, [(11)C]1) and D-luciferin [(11)C]methyl ether ([(11)C]LMEther, [(11)C]2) were synthesized in 25-55% radiochemical yield. PET studies with [(11)C]LMEster and [(11)C]LMEther demonstrate a lower retention of the C-11 label at 45 min post-injection in luciferase expression tumor. Optical imaging with unlabeled substrate D-luciferin and radiotracers [(11)C]LMEster and [(11)C]LMEther gave tumor luciferase images within a few minutes of photon counting. 相似文献
20.
Cesium-137 (137Cs) is one of the most important nuclear fission elements that contaminated the environment after the explosion of the Chernobyl nuclear power plant in Ukraine (1986). The aim of the study was to compare the efficacy of two chelating agent, Prussian blue and apple-pectin on 137cesium decorporation in rats. Rats were intravenously injected with a solution of 137cesium (5 kBq per rat). Chelating agents, Prussian blue or apple-pectin were given immediately after Cs contamination and during 11 days by addition of each chelating agent in drinking water at a concentration corresponding to 400 mg kg(-1) day(-1). Efficiency was evaluated 11 days after contamination (at the end of treatment) through their ability to promote Cs excretion and to reduce the radionuclide accumulation in some retention compartments (blood, liver, kidneys, spleen, skeleton and in the remaining carcass). In these conditions after treatment with Prussian blue a fivefold increase in fecal excretion of Cs was observed and was associated with a reduction in the radionuclide retention in the main organs measured. In contrast, no significant differences were observed between untreated rats and rats treated with apple-pectin. These observations were discussed in terms of ability of pectins to bind Cs and compared to recently published results obtained after treatment of Cs-contaminated children with this chelate. 相似文献