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PubMed2003

Nitrosative stress induced cytotoxicity in Giardia intestinalis.

AIMS: To investigate the antigiardial properties of the nitrosating agents: sodium nitrite, sodium nitroprusside and Roussin's black salt. METHODS AND RESULTS: Use of confocal laser scanning microscopy and flow cytometry indicated permeabilization of the plasma membrane to the anionic fluorophore, DiBAC4(3) [bis(1,3-dibutylbarbituric acid) trimethine oxonol]. Loss of plasma membrane electrochemical potential was accompanied by loss of regulated cellular volume control. Changes in ultrastructure revealed by electron microscopy and capacity for oxygen consumption, were also consequences of nitrosative stress. Roussin's black salt (RBS), active at micromolar concentrations was the most potent of the three agents tested. CONCLUSIONS: These multitargeted cytotoxic agents affected plasma membrane functions, inhibited cellular functions in Giardia intestinalis and led to loss of viability. SIGNIFICANCE AND IMPACT OF THE STUDY: Nitrosative damage, as an antigiardial strategy, may have implications for development of chemotherapy along with suggesting natural host defence mechanisms.

Animals↗
PubMed2002

Flux through multicellular layers of a technetium-99m-nitroimidazole for imaging hypoxia.

BRU59-21 is a technetium-99m-nitroimidazole being investigated as a noninvasive marker of tumor hypoxia. Metabolic depletion of BRU59-21, which is used at picomolar concentrations, could limit its ability to reach all hypoxic tumor cells. The multicellular layer (MCL) system, an in vitro model of the extravascular space, was used to assess the ability of BRU59-21 to diffuse to, and beyond, the target population of hypoxic cells. The flux of radioactivity through the MCL system was dependent on the oxygen concentration in the gas phase. Decreased flux and increased metabolism of BRU59-21 were observed under hypoxic compared with aerobic conditions. Analysis of the radioactivity, which passes through the hypoxic MCL, revealed that a proportion of the radioactivity was unmetabolized BRU59-21, but a significant fraction was free pertechnetate. The oxygen dependency of the flux of BRU59-21 required the presence of the nitroimidazole group and was not observed at 4 degrees C, indicating an enzymatic process is required to observe this effect. These findings suggest that metabolic depletion of BRU59-21 is not a major limit to its ability to reach hypoxic cells, but drug metabolism resulting in release of the radioactive label may reduce the ability of BRU59-21 to selectively label hypoxic cells in solid tumors.

Cell Hypoxia↗
PubMed1994

Mechanism of inhibition of FaDu hypopharyngeal carcinoma cell growth by tetraphenylphosphonium chloride.

Cationic phosphonium salts are interesting because they inhibit the proliferation of carcinoma cells more than untransformed epithelial cells in vitro. This differential anti-proliferative effect has been used to identify phosphonium salts and other lipophilic cations that later demonstrated effects in animals. Using 6 carcinoma-derived and 2 untransformed epithelial cell lines, tetraphenylphosphonium chloride (TPP) and other cationic aryl phosphonium salts (CAPS) demonstrated a growth inhibition pattern similar to that of cation rhodamine 123, suggesting that CAPS may inhibit mitochondrial function. We tested this hypothesis for the effect of phosphonium salt TPP on FaDu human hypopharyngeal carcinoma cells. TPP inhibited the proliferation of FaDu carcinoma cells at submicromolar concentrations. Uptake of 3H-TPP by FaDu cells was partially inhibited in medium containing high K+ and fully inhibited by valinomycin in this medium, indicating that TPP accumulates preferentially in mitochondria, and to a lesser extent in the cytoplasm. FaDu cells exposed to TPP exhibited damage to mitochondrial inner membranes, reduced ATP/ADP ratios, decreased oxygen uptake rates and decreased mitochondrial membrane potentials. The treated cells secreted lactate more rapidly than untreated controls and exhibited hypersensitivity to 2-deoxyglucose, an inhibitor of glycolysis. TPP's antimitochondrial effects apparently enhance cytoplasmic glycolysis. In conclusion, TPP inhibits FaDu carcinoma cell growth by inhibiting mitochondrial respiration and ATP synthesis. Cationic phosphonium salts that inhibit carcinoma cell growth through antimitochondrial effects might be used to treat solid tumors without the risk of secondary tumors associated with agents affecting nuclear DNA.

Animals↗
PubMed2004

Electron microscopic evaluation of the endothelial surface layer of glomerular capillaries.

Recent data from various vascular beds suggest that a layer of mucopolysaccharides covering the endothelial cells play an important role in transport processes, among others. In this study, electron microscopy (EM) was used to explore the presence of an endothelial surface layer (ESL) in rat glomerular capillaries. We adopted various fixation and labeling techniques, as follows: (1) negatively charged lipid particles were used as a tracer that was expected to be excluded from the ESL. The density of intravascular lipid particles in flow-arrested capillaries was 89% lower in a 200-nm periendothelial area than in the rest of the luminal space (n = 6 rats, P < 0.001); (2) podocytes of cryofixed fresh tissue had a 20-nm extramembranous coat, interpreted as the true glycocalyx; the coat was less expressed on the endothelium; (3) on unfixed endothelial cells, colloidal lanthanum labeled a 60-nm-thick layer, occasionally forming lumps; (4) perfusion with a fluorocarbon-based oxygen-carrying fixative, followed by tannic acid contrast enhancement, revealed an extensive (> 200 nm) ESL not previously described; however, this finding was restricted to superficial glomerular capillaries; (5) Cupromeronic Blue cytochemistry displayed a loose proteoglycan network in fenestral openings and, occasionally, a semiordered ESL; (6) ferricyanide-reduced osmication resulted in increased numbers of fenestral diaphragms. In conclusion, this study provides novel morphological evidence to support the presence of a significant glomerular ESL.

Animals↗
PubMed1993

Hemodynamic mechanisms of the antianginal action of a novel vasodilator FK409 in dynamic exercise-induced angina.

FK409 is a novel vasodilator with a unique chemical structure. We wished to elucidate the mechanisms of antianginal action of FK409 in dynamic exercise-induced angina. Twelve patients with stable effort angina pectoris were studied before and after a single 40-mg oral dose of FK409. Chest pain was induced in all of 12 patients during the control multistage bicycle ergometer exercise. After FK409 administration, the same workload did not induce chest pain in 6 patients. The ST segment at peak exercise showed less severe depression from 0.15 +/- 0.02 to 0.05 +/- 0.01 mV (p < 0.001). Left ventricular (LV) filling estimated by the Doppler method was reduced, and pulmonary artery wedge pressure decreased significantly (p < 0.001) throughout exercise testing after FK409. Myocardial oxygen uptake and coronary sinus flow throughout exercise testing decreased significantly (p < 0.05) after FK409 administration. The results of the present study demonstrate that decrease in myocardial oxygen demand may be caused by pre- and afterload reduction and that it could be a major mechanism of the antianginal action of FK409. However, other mechanisms such as redistribution of coronary blood flow to the subendocardium, direct dilatation of the stenotic parts of the epicardial arteries, and an increase in collateral blood flow should be considered additional possible mechanisms of the antianginal action of FK409.

Aged↗
PubMed2003

Electron paramagnetic resonance assessment of brain tissue oxygen tension in anesthetized rats.

UNLABELLED: The adequacy of cerebral tissue oxygenation (PtO(2)) is a central therapeutic end point in critically ill and anesthetized patients. Clinically, PtO(2) is currently measured indirectly, based on measurements of cerebrovascular oxygenation using near infrared spectroscopy and experimentally, using positron emission tomographic scanning. Recent developments in electron paramagnetic resonance (EPR) oximetry facilitate accurate, sensitive, and repeated measurements of PtO(2). EPR is similar to nuclear magnetic resonance but detects paramagnetic species. Because these species are not abundant in brain (or other tissues) in vivo, oxygen-responsive paramagnetic lithium phthalocyanine crystals implanted into the cerebral cortex are used for the measurement of oxygen. The line widths of the EPR spectra of these materials are linear functions of PtO(2). We used EPR oximetry in anesthetized rats to study the patterns of PtO(2) during exposure to various inhaled and injected general anesthetics and to varying levels of inspired oxygen. Rats anesthetized with 2.0 minimum alveolar anesthetic concentration isoflurane maintained the largest PtO(2) (38.0 +/- 4.5 mm Hg) and rats anesthetized with ketamine/xylazine had the smallest PtO(2) (3.5 +/- 0.3 mm Hg) at a fraction of inspired oxygen (FIO(2)) of 0.21, P < 0.05. The maximal PtO(2) achieved under ketamine/xylazine anesthesia with FIO(2) of 1.0 was 8.8 +/- 0.3 mm Hg, whereas PtO(2) measured during isoflurane anesthesia with FIO(2) of 1.0 was 56.3 +/- 1.7 mm Hg (P < 0.05). These data highlight the experimental utility of EPR in measuring PtO(2) during anesthesia and serve as a foundation for further study of PtO(2) in response to physiologic perturbations and therapeutic interventions directed at preventing cerebral ischemia. IMPLICATIONS: Using in vivo electron paramagnetic resonance oximetry, we studied the patterns of cerebral tissue oxygenation (PtO(2)) during exposure to various inhaled and injected general anesthetics, and to varying levels of inspired oxygen. These data show that inhaled anesthetics result in larger levels of PtO(2) in the brain than do several injectable anesthetics. The results highlight the experimental utility of electron paramagnetic resonance in measuring PtO(2) during anesthesia and serve as a foundation for further study of PtO(2) in response to physiologic perturbations and therapeutic interventions directed at preventing cerebral ischemia.

Anesthesia↗
PubMed1985

[Effects of lead poisoning on properties of brain mitochondria in young rats].

When the litters were 14 days old, wistar rat pups received lead ions. The suckling mother was fed by a powdered laboratory chow containing lead carbonate (1%, 2%, 4%). The intoxication was going on for 3 days to 9 weeks. While lead-fed pups showed a decrease in body-weight gain and in neurologic development, lead ions were without effects on oxygen consumption, ADP-phosphorylation and activity of several enzymes of cerebral mitochondria. On the other hand, the important lead accumulation into cerebral mitochondria was in a straight ratio with lead doses in the feedings. To explain the in vivo data, the effects of lead acetate were investigated in vitro on brain mitochondria of young male wistar rats. Our findings indicate that lead ions alter mitochondrial respiration and ADP-phosphorylation and that inorganic phosphate has a protective effect.

Animals↗
PubMed1980

Changes in contractile function and endogenous fuel supply in rat heart upon perfusion with substrate-free medium.

Isolated rat hearts were perfused with aerobic substrate-free medium for different intervals during which changes in functional and metabolic events were examined. The contractile force was maintained for 30 min but thereafter declined toward zero over a period of 90 min. Before the onset of contractile failure, glycogen decreased by 60% of the control value, various intermediates of glycolytic flux, hexosephosphates, and triosephosphates, except dihydroxyacetone phosphate, reached their lowest level, and hydration of the myocardium became maximal. Furthermore, the phosphate potential, creatine phosphate (CrP), ATP, and oxygen consumption decreased by 60%, 45%, 10%, and 18%, respectively, before the onset of contractile failure. A progressive decrease in citrate, isocitrate, alpha-ketoglutarate, and malate was observed during a 2-hr perfusion period, but a slight increase in the levels of oxaloacetate and acetyl-CoA was apparent at 30 and 60 min, respectively. The early phase of contractile failure (30-60 min) was associated with an increase in the free fatty acid (FFA) and AMP levels, whereas the late phase (90-120 min) was characterized by an increase in resting tension and a decrease in oxygen consumption. The complete failure of the heart to generate contractile force at 120 min of perfusion occurred when about 40% of the glycogen and ATP contents and about 25% of the creatine phosphate and triglyceride contents were still present. Therefore, contractile failure of the hearts perfused with substrate-free medium may be caused by an insufficiency of the mechanisms responsible for the mobilization of endogenous glycogen and triglycerides as well as for the generation and utilization of ATP.

Acetyl Coenzyme A↗
PubMed2001

The role of redox-active amino acids on compound I stability, substrate oxidation, and protein cross-linking in yeast cytochrome C peroxidase.

The role of two tryptophans (Trp51 and Trp191) and six tyrosines (Tyr36, Tyr39, Tyr42, Tyr187, Tyr229, and Tyr236) in yeast cytochrome c peroxidase (CcP) has been probed by site-directed mutagenesis. A series of sequential mutations of these redox-active amino acid residues to the corresponding, less oxidizable residues in lignin peroxidase (LiP) resulted in an increasingly more stable compound I, with rate constants for compound I decay decreasing from 57 s(-1) for CcP(MI, W191F) to 7 s(-1) for CcP(MI, W191F,W51F,Y187F,Y229F,Y236F,Y36F,Y39E,Y42F). These results provide experimental support for the proposal that the stability of compound I depends on the number of endogenous oxidizable amino acids in proteins. The higher stability of compound I in the variant proteins also makes it possible to observe its visible absorption spectroscopic features more clearly. The effects of the mutations on oxidation of ferrocytochrome c and 2,6-dimethoxyphenol were also examined. Since the first mutation in the series involved the change of Trp191, a residue that plays a critical role in the electron transfer pathway between CcP and cyt c, the ability to oxidize cyt c was negligible for all mutant proteins. On the other hand, the W191F mutation had little effect on the proteins' ability to oxidize 2,6-dimethoxyphenol. Instead, the W51F mutation resulted in the largest increase in the k(cat)/K(M), from 2.1 x 10(2) to 5.0 x 10(3) M(-1) s(-1), yielding an efficiency that is comparable to that of manganese peroxidase (MnP). The effect in W51F mutation can be attributed to the residue's influence on the stability and thus reactivity of the ferryl oxygen of compound II, whose substrate oxidation is the rate-determining step in the reaction mechanism. Finally, out of all mutant proteins in this study, only the variant containing the Y36F, Y39E, and Y42F mutations was found to prevent covalent protein cross-links in the presence of excess hydrogen peroxide and in the absence of exogenous reductants. This finding marks the first time a CcP variant is incapable of forming protein cross-links and confirms that one of the three tyrosines must be involved in the protein cross-linking.

Animals↗
PubMed2003

Asymmetric synthesis of oxygen heterocycles via Pd-catalyzed dynamic kinetic asymmetric transformations: application to nucleosides.

Racemic butadiene and isoprene monoepoxide react with unsaturated alcohols in the presence of a chiral palladium catalyst and a boron co-catalyst to give 3-alkoxy-4-hydroxy-1-butene and 3-alkoxy-4-hydroxy-3-methyl-1-butene, respectively, with excellent regio- and enantioselectivity in a dynamic kinetic asymmetric transformation whereby both enantiomers of the starting epoxides provide the same enantiomeric product. In the case of 2-phenylbutadiene monoepoxide, easily available from phenacyl chloride and vinylmagnesium bromide, the reaction proceeds by kinetic resolution. A model to rationalize the result is presented. The bis-olefin products are ideal substrates for the Ru catalyzed ring closing metathesis. In this way, five-, six-, and seven-membered oxygen heterocycles are readily available enantiomerically pure. The value of this very simple two step process is demonstrated by the use of the five-membered ring heterocycles to form unnatural and unusual nucleosides that cannot be easily accessed by other means. The sequence involves a Ru catalyzed isomerization of the initial 2,5-dihydrofuran to a 2,3-dihydrofuran followed by a selenium promoted addition of a pyrimidine or purine base. One advantage of this strategy is the easy access to either enantiomeric series, both of which have important biological applications.

Alcohols↗
PubMed1990

Cytotoxicity of a low molecular weight Cu2Zn2 superoxide dismutase active center analog in human erythroleukemia cells.

The cytotoxicity of SOD-mimics was studied in human K562 erythroleukemia cells. CuPUPY, a low molecular weight copper complex with properties typical of a Cu2Zn2 SOD active center analog was shown to display pronounced toxicity upon incubation with human K562 erythroleukemia cells, while the ligand, CuSO4 or CuEDTA did not affect vitality. Externally added catalase decreased the cytotoxic effects of CuPUPY by 50% indicating an involvement of hydrogen peroxide in toxicity. An increased oxygen uptake and glutathione oxidation by K562 cells in the presence of CuPUPY suggested that toxicity might be due to a copper-mediated redox-cycle. In fact addition of glutathione to a solution of CuPUPY resulted in glutathione oxidation, O2-consumption and H2O2-generation. CuPUPY proved to be less toxic to human lymphocytes than to K562 cells. This selectivity may be related to the low content of antioxidative enzymes in K562 cells.

Binding Sites↗
PubMed1976

The effects of diphenyleneiodonium and of 2,4-dichlorodiphenyleneiodonium on mitochondrial reactions. Mechanism of the inhibition of oxygen uptake as a consequence of the catalysis of the chloride/hydroxyl-ion exchange.

1. Increasing the substrate concentration only decreased the inhibition of mitochondrial oxidations by diphenyleneiodonium or by 2,4-dichlorophenyleneiodonium by a small amount. 2. Diphenyleneiodonium and 2,4-dichlorodiphenyleneiodonium lowered the amounts of succinate, citrate and glutamate accumulated in the matrix of mitochondria in the presence of Cl-, but not in its absences. 2,4-Dichlorodiphenyleneiodonium decreased the accumulation of substrates by mitochondria oxidizing glycerol 3-phosphate. 3. Diphenyleneiodonium caused an alkalinization of the medium with an anaerobic suspension of mitochondria, which was only partly reversed by Triton X-100. 4. The rate of proton extrusion by mitochondria oxidizing succinate was not altered by diphenyleneiodonium or by 2,4-dichlorodiphenyleneiodium, although the rate of decay of proton pulses was increased. 5. 2,4-Dichlorodiphenyleneiodonium shifted the pH optimum for succinate oxidation by intact mitochondria from pH 7.2 to 8.0, whereas there was no effect on that of freeze-thawed mitochondria, which was pH 8.0. 6. The concentration of 2,4-dichlorophenyleneiodonium required to inhibit respiration by 50% is less the higher the absolute rate of oxygen uptake. 7. EDTA, but not EGTA [ethanedioxybis(ethylamine)-tetra-acetic acid] increased the inhibition of respiration by diphenyleneiodonium, 2,4-dichlorodiphenyleneiodonium and by tri-n-propyltin. 8. It is concluded that diphenyleneiodonium and 2,4-dichlorodiphenyleneiodonium limit respiration in Cl--containing medium by causing an acidification of the matrix, and that there are pH-sensitive sites in the respiratory chain between NADH and succinate, and between succinate and cytochrome c.

Animals↗
PubMed1993

Inhibition of phthalocyanine-sensitized photohemolysis of human erythrocytes by quercetin.

Photohemolysis of erythrocytes in the presence of aluminum phthalocyanine tetrasulfonate as a sensitizer is inhibited by quercetin. D2O (98.5%) stimulated photohemolysis regardless of quercetin presence, suggesting the participation of singlet oxygen in the process. Since it has been shown that this flavonoid reacts with singlet oxygen, the protective effect might be attributed, at least partially, to its competitive reaction with singlet oxygen. At the molecular level, the alterations of membrane proteins that escort the process of photohemolysis, such as cross-linking of spectrin monomers and of other membrane proteins, were selectively inhibited by quercetin. This effect was qualitatively similar to that induced by NaF, suggesting that quercetin may, like NaF, also inhibit type I photooxidations, which contribute to hemolysis. The lipophilicity of quercetin seems to be an essential factor in the inhibition process; rutin, a water-soluble 3-rutinoside of quercetin, had only a negligible protective effect on photohemolysis.

Erythrocytes↗
PubMed2001

Evidence for a role of salicylic acid in the oxidative damage generated by NaCl and osmotic stress in Arabidopsis seedlings.

Previous studies have shown that salicylic acid (SA) is an essential component of the plant resistance to pathogens. We now show that SA plays a role in the plant response to adverse environmental conditions, such as salt and osmotic stresses. We have studied the responses of wild-type Arabidopsis and an SA-deficient transgenic line expressing a salicylate hydroxylase (NahG) gene to different abiotic stress conditions. Wild-type plants germinated under moderate light conditions in media supplemented with 100 mM NaCl or 270 mM mannitol showed extensive necrosis in the shoot. In contrast, NahG plants germinated under the same conditions remained green and developed true leaves. The lack of necrosis observed in NahG seedlings under the same conditions suggests that SA potentiates the generation of reactive oxygen species in photosynthetic tissues during salt and osmotic stresses. This hypothesis is supported by the following observations. First, the herbicide methyl viologen, a generator of superoxide radical during photosynthesis, produced a necrotic phenotype only in wild-type plants. Second, the presence of reactive oxygen-scavenging compounds in the germination media reversed the wild-type necrotic phenotype seen under salt and osmotic stress. Third, a greater increase in the oxidized state of the glutathione pool under NaCl stress was observed in wild-type seedlings compared with NahG seedlings. Fourth, greater oxidative damage occurred in wild-type seedlings compared with NahG seedlings under NaCl stress as measured by lipid peroxidation. Our data support a model for SA potentiating the stress response of the germinating Arabidopsis seedling.

Arabidopsis↗
PubMed2001

A photobiological and photophysical-based study of phototoxicity of two chlorins.

To understand the fundamental determinants of phototoxic efficacy and absorbed photodynamic dose, the triplet state and photobleaching quantum yields in living cells, cellular uptake, intracellular localization, and correlation with cell viability were studied for the two purpurins tin ethyl etiopurpurin 1 (SnET2) and tin octaethylbenzochlorin (SnOEBC) in ovarian cancer cells (OVCAR5). Although the triplet yields of these two photosensitizers were not significantly affected by cellular incorporation, the photobleaching yields were shown to be 3 orders of magnitude higher for cellular-bound sensitizer than for free or albumin-bound photosensitizer and higher for SnET2 than for SnOEBC for all of the cases. The intracellular concentration of SnOEBC was half that of SnET2 after 3 h- and 24 h-incubation times for both 0.1 microM and 1.0 microM incubation concentrations. Despite the lower concentrations of SnOEBC, the phototoxicity of the two photosensitizers was comparable at 1-microM incubation concentration and was up to 10-fold higher for SnOEBC at the lower concentration. The subcellular localization established using confocal microscopy and molecular probes showed that both photosensitizers were primarily lysosomally localized. SnOEBC, however, had an extra-lysosomal, mitochondrial localization component. The photophysical measurements allowed calculation of the intracellular singlet oxygen production, which indicated that the photosensitizer-light dose reciprocity was limited by photobleaching for SnET2 but only minimally for SnOEBC, and this was confirmed through cell-survival studies. Taken together, these data indicate that the critical determinant of differences in phototoxicity between the two molecules was their relative rates of photobleaching and their subcellular localization. The study points to the importance of combining photosensitizer uptake and localization with photophysical measurements in the relevant biological milieu to reasonably interpret and/or predict photosensitization efficacies.

Cell Survival↗
PubMed1987

The mechanism of acute cytotoxicity of triethylphosphine gold(I) complexes. I. Characterization of triethylphosphine gold chloride-induced biochemical and morphological changes in isolated hepatocytes.

Triethylphosphine gold complexes are effective therapeutic agents used for the treatment of rheumatoid arthritis. Many of those molecules are also highly cytotoxic in vitro and can inhibit DNA and protein synthesis. Preliminary experiments have indicated that triethylphosphine gold chloride (TEPAu) may induce the peroxidative decomposition of cellular membrane lipids. The purpose of these investigations therefore was to evaluate the role of lipid peroxidation in the mechanism of acute cytotoxicity of a gold(I) coordination complex, TEPAu, and to examine the early morphological and biochemical changes induced by TEPAu in suspensions of freshly isolated rat hepatocytes. TEPAu caused a rapid loss of cell viability at concentrations above 25 microM which was significantly different from that of control by 60 min and complete by 180 min of incubation. TEPAu also depleted cells of reduced glutathione (GSH) and increased the formation of malondialdehyde (MDA) by 60 min. Incubation of cells with either of the antioxidants, N,N'-diphenyl-p-phenylenediamine (DPPD) or promethazine blocked the formation of MDA but did not alter the time course of cell death or GSH depletion induced by TEPAu. TEPAu also caused a decrease in cellular NADPH and NADH by 10 min. Electron microscopy of hepatocytes exposed to TEPAu revealed early (5 min) formation of flocculent electron-dense precipitates within condensed mitochondria. These changes characteristically preceded cell death. Energy-dispersive electron-probe microanalysis indicated that the electron-dense precipitates did not contain detectable amounts of gold. TEPAu also caused a concentration-dependent decrease in cellular ATP and oxygen consumption in isolated rat hepatocytes. These data suggest that lipid peroxidation, as indicated by the formation of MDA, is probably not a major mechanism by which triethylphosphine gold complexes lethally injure cells. These data, therefore, suggest that mitochondria may be target organelles in TEPAu-induced toxicity to isolated rat hepatocytes.

Animals↗
PubMed2005

Hydroxylamines as oxygen atom nucleophiles in transition-metal-catalyzed allylic substitution.

[reaction: see text] The viability of hydroxylamines as nucleophiles in transition-metal-catalyzed allylic substitutions was examined. We have found that the oxygen atom of hydroxylamines having an N-electron-withdrawing substituent (also known as hydroxamic acids) acts as a reactive nucleophile. The palladium-catalyzed O-allylic substitution of hydroxylamines with allylic carbonate afforded the linear hydroxylamines. The selective formation of the branched hydroxylamines was observed in iridium-catalyzed reaction. Regio- and enantioselective allylic substitution of the unsymmetrical phosphates with hydroxylamines was studied by using the iridium complex of chiral pybox ligand. The aqueous-medium reaction with hydroxylamines proceeded smoothly in the presence of Ba(OH)(2).H(2)O to give the branched products with good enantioselectivities.

Allyl Compounds↗
PubMed1998

Nitrogen, sulfur and oxygen donor adducts with copper(II) complexes of antitumor 2-formylpyridinethiosemicarbazone analogs: physicochemical and cytotoxic studies.

The preparation of N-, S- and O-donor ligand adducts with CuX+ (HX = 6-methyl-2-formylpyridinethiosemicarbazone (6HL); 2-formylpyridine-2'-methylthiosemicarbazone (2'L); 2-formylpyridine-4'-methylthiosemicarbazone (4'HL) is described. The N-donors, 2,2'-bipyridyl (bipy), 4-dimethylaminopyridine (dmap) give the complexes [Cu(6L)(bipy)]PF6, [Cu(6L)(bipy)]Cl.5H2O, [Cu(4'L)(bipy)]PF6, [Cu(6L)(dmap)2]PF6.2.5 H2O and [Cu(4'L)(dmap)2]PF6.H2O which have been characterized by physical and spectroscopic techniques. Pentafluorothiophenolate (pftp) gives S-donor complexes [CuX(pftp)] (X = 6L and 4'L) and thiolato co-ordination is proposed on the basis of spectroscopic evidence. Paratritylphenolate (ptp) and HPO4(2-) give O-donor complexes [Cu(6L)(ptp)], [Cu(4'L)(ptp)], [¿Cu(6L)¿2HPO4].4H2O, and [¿Cu(4'L)¿2HPO4].5H2O which have been characterized by physical and spectroscopic techniques, as have the precursor complexes [Cu(6L)(CH3COO)].H2O, [Cu(4'L)(CH3COO)], Cu(6HL)(CF3COO)](CF3COO).0.5H2O, [Cu(4'HL)(CF3COO)](CF3COO), [Cu(2'L)Cl2) and [Cu(2'L)(NO3)2]. Protonation constants for the ligands and some of their complexes have been determined. 2-Formylpyridinethiosemicarbazone (HL) complexes of silver, gold, zinc, mercury, cadmium and lead are also discussed. Cytotoxicity against the human tumor cell line HCT-8 and antiviral data for selected compounds are presented.

Animals↗