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81.
Cardiac troponin T following repeated administration of pyridoxal isonicotinoyl hydrazone in rabbits
Adamcová M Machácková J Gersl V Pelouch V Simůnek T Klimtová I Hrdina R Ponka P 《Physiological research / Academia Scientiarum Bohemoslovaca》2002,51(5):443-448
Pyridoxal isonicotinoyl hydrazone (PIH) is a new tridentate Fe-chelating agent that should be very promising in many pathological states resulting from both an iron-overload and formation of free radicals. The aim of our study was to investigate the effect of PIH on the cardiovascular system focusing to the regulatory protein -- cardiac troponin T (cTnT). The study was carried out in two groups of Chinchilla male rabbits: 1) PIH (50 mg/kg dissolved in 10 % Cremophor i.p., once a week, 10 administrations, n=8) and 2) Cremophor (2 ml/kg i.p. in the same schedule, n=7). Plasma concentrations of cTnT (as a marker of myocardial damage) were measured using a commercial kit (Roche). cTnT was within the physiological range (i.e. < 0.1 microg/l) during the whole experiment in the Cremophor group. In the PIH group, the cTnT levels were not significantly increased when compared with the control group or with the initial values (except with those before the 5th administration). Furthermore, we analyzed the cytosolic and myofibrillar fraction of cTnT in the left ventricular myocardium. Using SDS-PAGE and Western blot we resolved three isoforms. The profiling of TnT did not differ significantly between the PIH-treated group and the Cremophor-treated group. Our data concerning cTnT support the opinion that the possible cardiotoxicity of PIH is very low. 相似文献
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Allen R. Huang Premysl Ponka 《Biochimica et Biophysica Acta (BBA)/General Subjects》1983,757(3):306-315
Pyridoxal isonicotinoyl hydrazone (PIH) has recently been identified as a new iron chelating agent with a high degree of iron mobilizing activity in vitro and in vivo which makes this compound a candidate drug in the treatment of iron overload. This study was undertaken to elucidate the mechanism of action of the iron mobilizing activity of PIH at the cellular level. An in vitro system of rabbit reticulocytes with a high level of non-heme 59Fe was used as a model of iron overload. The effects of various biochemical and physiological manoeuvers on the mobilization of 59Fe by PIH from the cells were studied. The fate of [14C]-PIH in the in vitro system was also studied. Studies were also carried out using a crude mitochondrial fraction. The results indicate three phases of the iron mobilizing activity of PIH: (1) the entry of PIH into erythroid cells seems to be by passive diffusion; (2) chelation occurs mainly from mitochondria and may depend on the availability of iron in a low molecular weight, non-heme pool. Chelation seems to be enhanced by reduction of Fe (III) to Fe (II); (3) the exit of the PIH2-Fe complex is an energy-dependent process. Iron mobilization by PIH is not dependent on (Na+ + K+)-ATPase activity, external ionic composition, or external hydrogen ion concentration. Membrane fluidity does not seem to play a role in PIH-Fe mobilization. The exit of the PIH2-Fe complex is inhibited by anti-microtubule agents (vinca alkaloids but not colchicine)_suggesting that the PIH2-Fe complex is actively extruded from the cell by a microtube-dependent event. 相似文献
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Premysl Ponka Herbert M. Schulman Ania Wilczynska 《Biochimica et Biophysica Acta (BBA)/General Subjects》1982,718(2):151-156
We have examined whether reticulocytes depleted of transferrin might incorporate 59Fe from 59Fe-labelled pyridoxan isonicotinoyl hydrazone (PIH). Transferrin-depleted reticulocytes showed a time-, temperature- and concentration-dependent incorporation of 59Fe when incubated with 20–200 μM 59Fe-PIH. The amount of 59Fe incorporated with 200 μM 59Fe-PIH is equal to or higher than that taken up from transferrin at 20 μM 59Fe concentration. After 60 min about 60% of the 59Fe taken up by the cells is recovered in heme while the remainder is probably still bound to PIH. 1 mM succinyl acetone (a specific inhibitor of heme synthesis) inhibits PIH-mediated incorporation of 59Fe into heme by about 79% indicating that 59Fe from 59Fe-PIH is incorporated into de novo synthesized protoporphyrin. As is the case with transferrin, erythrocytes do not incorporate 59Fe from 59Fe-PIH. Pretreatment of reticulocytes with pronase does not inhibit their ability to incorporate 59Fe from 59Fe-PIH, suggesting that, unlike the uptake of Fe from transferrin, membrane receptors are not involved in the uptake of Fe-PIH by the cells. 相似文献
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Premysl Pejchar Roman Pleskot Katerina Schwarzerová Jan Martinec Olga Valentová Zuzana Novotná 《Cell biology international》2008,32(5):554-556
Aluminum is a highly cytotoxic metal to plants, but the molecular base and the primary target of Al toxicity are still unknown. The most important physiological consequence of Al toxicity is a cessation of root growth and changes in root morphology suggesting a role of the root cytoskeleton as a target structure. The important role of phospholipid degrading enzyme phospholipase D in regulation of cytoskeleton remodelling in both animal and plant organisms is now evident. Both the phospholipid pathway and the cytoskeleton are influenced by Al(3+), but their relationship with Al stress remains to be explored. Therefore, we tested the possibility that Al stress could be sensed by plants through microtubules in close interaction with phospholipases. We have shown that Al(3+) reduced the formation of phosphatidic acid in vivo, inhibited activity of phosphatidylinositol-4,5-bisphosphate-dependent phospholipase D in vitro and that the phosphatidic acid production is modified by microtubule dynamics. 相似文献
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