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1.
A study conducted on Fe 2+ autoxidation showed that its rate was extremely slow at acidic pH values and increased by increasing the pH; it was stimulated by Fe 3+ addition but the stimulation did not present a maximum at a Fe 2+/Fe 3+ ratio approaching 1:1. The species generated during Fe 3+-catalyzed Fe 2+ autoxidation was able to oxidize deoxyribose; the increased Fe 2+ oxidation observed at higher pHs was paralleled by increased deoxyribose degradation. The species generated during Fe 3+-catalyzed Fe 2+ autoxidation could not initiate lipid peroxidation in phosphatidylcholine liposomes from which lipid hydroperoxides (LOOH) had been removed by treatment with triph-enylphosphine. Neither Fe 2+ oxidation nor changes in the oxidation index of the liposomes due to lipid peroxidation were observed at pHs where the Fe 3+ effect on Fe 2+ autoxidation and on deoxyribose degradation was evident. In our experimental system, a Fe 2+/Fe 3+ ratio ranging from 1:3 to 2:1 was unable to initiate lipid peroxidation in LOOH-free phosphatidylcholine liposomes. By contrast Fe 3+ stimulated the peroxidation of liposomes where increasing amounts of cumene hydroperoxide were incorporated. These results argue against the participation of Fe 3+ in the initiation of LOOH-independent lipid peroxidation and suggest its possible involvement in LOOH-dependent lipid peroxidation. 相似文献
2.
1. The amplitudes of the fast (0–20 μs) and slow (20 μs–2 ms) fluorescence rise induced by a 2 μs flash have been measured as a function of the energy of the flash in chloroplasts inhibited by 3(3,4-dichlorophenyl)-1,1-dimethylurea. The saturation curve for the slow rise shows a characteristic lag which is not observed for the fast fluorescence rise. This lag indicates that Photosystem II centers undergo a double hit process which implies that (a), each photocenter includes two acceptors Q 1 and Q 2; (b), after the first hit, oxidized chlorophyll Chl + is reduced by a secondary acceptor Y in a time short compared to the duration of the flash; (c), after the second hit, Chl + is reduced by another secondary donor, D. 2. According to Den Haan et al. ((1974) Biochim. Biophys. Acta 368, 409–421), hydroxylamine destroys the secondary donor responsible for the fast reduction of Chl+. In the presence of 3 mM hydroxylamine, only the secondary donor D is functional and a flash induces mainly a single hit process. 3. The saturation curves for the fast and the slow rises have been studied in the presence of 3(3,4-dichlorophenyl)-1,1-dimethylurea for a second actinic flash given 2.5 s after a first saturating one. The large decrease in the half-saturating energy indicates the existence of efficient energy transfer occuring between photosynthetic units. 4. Two alternate hypotheses are discussed (a) in which D is an auxiliary donor and (b) in which D is included in the main electron transfer chain. 相似文献
3.
Objective: Al 3+ stimulates Fe 2+ induced lipid oxidation in liposomal and cellular systems. Low-density lipoprotein (LDL) oxidation may render the particle atherogenic. As elevated levels of Al 3+ and increased lipid oxidation of LDL are found in sera of hemodialysis patients, we investigated the influence of Al 3+ on LDL oxidation.
Materials and methods: Using different LDL modifying systems (Fe 2+, Cu 2+, free radical generating compounds, human endothelial cells, hemin/H 2O 2 and HOCl), the influence of Al 3+ on LDL lipid and apoprotein alteration was investigated by altered electrophoretic mobility, lipid hydroperoxide-, conjugated diene- and TBARS formation.
Results: Al 3+ could stimulate the oxidizability of LDL by Fe 2+, but not in the other systems tested. Al 3+ and Fe 2+ were found to bind to LDL and Al 3+could compete with Fe 2+ binding to the lipoprotein. Fluorescence polarization data indicated that Al 3+ does not affect the phospholipid compartment of LDL.
Conclusions:The results indicate that increased LDL oxidation by Fe 2+ in presence of Al 3+ might be due to blockage of Fe 2+ binding sites on LDL making more free Fe 2+ available for lipid oxidation. 相似文献
4.
Chelation by citrate was found to promote the autoxidation of Fe 2+, measured as the disapperance of 1,10-phenanthroline-chelatable Fe 2+. The autoxidation of citrate--- 2+ could in turn promote the peroxidation of microsomal phospholipid liposomes, as judged by malondialdehyde formation. At low citrate---Fe 2+ ratios the autoxidation of Fe 2+ was slow and the formation of malondialdehyde was preceded by a lag phase. The lag phase evidence of this, linear initial rates of lipid peroxidation were obtained via the combination of citrate---Fe 2+ and citrate---Fe 3+, optimum activity occurring at a Fe 3+---Fe 2+ ratio of 1:1. Evidence is also presented to suggest that the superoxide and the hydrogen peroxide that are formed during the autoxidation of citrate---Fe 2+ can either stimulate or inhibit lipid peroxidation by affecting the yield of citrate---Fe 3+ from citrate---Fe 2+. No evidence was obtained for the participation of the hydroxyl radical in the initiation of lipid peroxidation by citrate---Fe 2+. 相似文献
5.
In an experimental system where both Fe 2+ autoxidation and generation of reactive oxygen species is negligible, the effect of FeCl 2 and FeCl 3 on the peroxidation of phosphatidylcholine (PC) liposomes containing different amounts of lipid hydroperoxides (LOOH) was studied; Fe 2+ oxidation, oxygen consumption and oxidation index of the liposomes were measured. No peroxidation was observed at variable FeCl 2/FeCl 3 ratio when PC liposomes deprived of LOOH by triphenyl-phosphine treatment were utilized. By contrast, LOOH containing liposomes were peroxidized by FeCl 2. The FeCl 2 concentration at which Fe 2+ oxidation was maximal, defined as critical Fe 2+ concentration [Fe 2+]*, depended on the LOOH concentration and not on the amount of PC liposomes in the assay. The LOOH-dependent lipid peroxidation was stimulated by FeCl 3, addition; the oxidized form of the metal increased the average length of radical chains, shifted to higher values the [Fe 2+]* and shortened the latent period. The iron chelator KSCN exerted effects opposite to those exerted by FeCl 3 addition. The experimental data obtained indicate that the kinetics of LOOH-dependent lipid peroxidation depends on the Fe 2+/Fe 3+ ratio at each moment during the time course of lipid peroxidation. The results confirm that exogenously added FeCl 3 does not affect the LOOH-independent but the LOOH-deendent lipid peroxidation; and suggest that the Feg, endogenously generated exerts a major role in the control of the LOOH-dependent lipid peroxidation. 相似文献
6.
Although considerably more oxidation-resistant than other P-type ATPases, the yeast PMA1 H +-ATPase of Saccharomyces cerevisiae SY4 secretory vesicles was inactivated by H 2O 2, Fe 2+, Fe- and Cu-Fenton reagents. Inactivation by Fe 2+ required the presence of oxygen and hence involved auto-oxidation of Fe 2+ to Fe 3+. The highest Fe 2- (100 μM) and H 2O 2 (100 mM) concentrations used produced about the same effect. Inactivation by the Fenton reagent depended more on Fe 2+ content than on H 2O 2 concentration, occurred only when Fe 2+ was added to the vesicles first and was only slightly reduced by scavengers (mannitol, Tris, NaN 3, DMSO) and by chelators (EDTA, EGTA, DTPA, BPDs, bipyridine, 1, 10-phenanthroline). Inactivation by Fe- and Cu- Fenton reagent was the same; the identical inactivation pattern found for both reagents under anaerobic conditions showed that both reagents act via OH ·. The lipid peroxidation blocker BHT prevented Fenton-induced rise in lipid peroxidation in both whole cells and in isolated membrane lipids but did not protect the H +-ATPase in secretory vesicles against inactivation. ATP partially protected the enzyme against peroxide and the Fenton reagent in a way resembling the protection it afforded against SH-specific agents. The results indicate that Fe 2+ and the Fenton reagent act via metal-catalyzed oxidation at specific metal-binding sites, very probably SH-containing amino acid residues. Deferrioxamine, which prevents the redox cycling of Fe 2+, blocked H +-ATPase inactivation by Fe 2+ and the Fenton reagent but not that caused by H 2O 2, which therefore seems to involve a direct non-radical attack. Fe-Fenton reagent caused fragmentation of the H +-ATPase molecule, which, in Western blots, did not give rise to defined fragments bands but merely to smears. 相似文献
7.
The Fe 3+-doxorubicin complex undergoes reactions that suggest that the complex self-reduces to a ferrous oxidized-doxorubicin free radical species. The Fe 3+-doxorubicin system is observed to reduce ferricytochrome c, consume O 2 and react with 2,2′-bipyridine. Bipyridine acts as a “ferrous ion scavenger” as it reacts with the ferrous ion produced by Fe 3+-doxorubicin self-reduction. In the absence of O 2, a ferrous doxorubicin complex accumulates. In the presence of oxygen, Fe 2+ recycles back to Fe 3+. The rates of these reactions were measured and the Fe 3+-doxorubicin self-reduction was determined to be the rate-determining step. The Fe 3+-doxorubicin induced inactivation of cytochrome c oxidase and NADH cytochrome c reductase on beef heart submitochondrial particles occurs at a rate similar to Fe 3+-doxorubicin self-reduction. Thus the rate at which damage to these mitochondrial enzymes occurs may be controlled by a nonezymatic Fe 3+-doxorubicin self-reduction. 相似文献
8.
To define the molecular mechanism(s) of carvedilol inhibition of lipid peroxidation we have utilized model systems that allow us to study the different reactions involved in this complex process.
Carvedilol inhibits the peroxidation of sonicated phosphatidylcholine liposomes triggered by FeCl 2 addition whereas atenolol, pindolol and labetalol are ineffective. The inhibition proved not to be ascribable (a) to an effect on Fe 2+ autoxidation and thus on the generation of oxygen derived radical initiators; (b) to the scavenging of the inorganic initiators O ·-2 and ·OH; (c) to an effect on the reductive cleavage of organic hydroperoxides by FeCl 2; (d) to the scavenging of organic initiators. The observations that (a) carvedilol effectiveness is inversely proportional to the concentration of FeCl 2 and lipid hydroperoxides in the assay; (b) the drug prevents the onset of lipid peroxidation stimulated by FeCl 3 addition and; (c) it can form a complex with Fe 3+, suggest a molecular mechanism for carvedilol action. It may inhibit lipid peroxidation by binding the Fe 3+ generated during the oxidation of Fe 2+ by lipid hydroperoxides in the substrate. The lag time that carvedilol introduces in the peroxidative process would correspond to the time taken for carvedilol to be titrated by Fe 3+; when the drug is consumed the Fe 3+ accumulates to reach the critical parameter that stimulates peroxidation. According to this molecular mechanism the antioxidant potency of carvedilol can be ascribed to its ability to bind a species, Fe 3+, that is a catalyst of the process and to its lipophilic nature that concentrates it in the membranes where Fe 3+ is generated by a site specific mechanism. 相似文献
9.
综述了近年趋磁细菌纳米磁小体生物合成的分子机制及应用进展。磁小体的合成涉及磁小体膜的形成、铁的吸收和转运、磁小体晶体的矿化、成熟以及磁小体的链状排列等。其中Mam J和Mam K互作并丝状排列,固定磁小体使其链状排列及磁小体膜由细胞质膜内陷而形成是两个令人注目的成就。我们也提出了关于磁小体的生理意义及合成机制的假说:细胞在低氧浓度下由于氧胁迫大量吸收铁,Fe 3+/Fe 2+电子对可起到类似O 2/H 2O的作用,产生能量并作为电子受体;Fe3+得到电子还原成的Fe 2+可引起Fenton反应,此反应产生的活性氧可影响到生物体的正常生理代谢,细胞为降低Fe 2+浓度,将其与Fe 3+一同转化为Fe 3O 4颗粒;磁小体的生理功能之一是降低胞内的活性氧。 相似文献
10.
Based on electron acceptor abundance, Fe 3+ and SO 42- reduction by bacteria may play a dominant role in intrinsic bioremediation of some organic contaminants in the subsurface. Both Fe 3+ and SO 42- reduction processes involve mineral phases and may not be properly understood by evaluating only groundwater concentrations. Fe and S mineral analyses should be incorporated in natural attenuation studies; however, inherent problems with sample collection and analysis have discouraged such efforts. Methods are presented here for (1) sediment collection and anoxic preservation, (2) evaluation of biologically available Fe 3+ and biogenically produced Fe 2+ minerals, and (3) a simplified extended mineral sulfide analysis for ∼FeS and S°+FeS 2. These techniques are demonstrated to evaluate Fe 3+ and SO 42- reduction at three sites where the soil or aquifer matrix had been contaminated with gasoline fuel, methane gas, or landfill leachate. It is expected that these techniques will permit Fe and S mineral analyses to become a routine part of natural attenuation assessments. 相似文献
11.
The effect of different oxygen radical-generating systems on NAD(P)H was determined by incubating the reduced forms of the pyridine coenzymes with either Fe 2+-H 2O 2 or Fe 3+-ascorbate and by analyzing the reaction mixtures using a HPLC separation of adenine nucleotide derivatives. The effect of the azo-initiator 2,2'-azobis(2-methylpropionamidine)dihydrochloride was also tested. Results showed that, whilst all the three free radical-producing systems induced, with different extent, the oxidation of NAD(P)H to NAD(P) +, only Fe 2+-H 2O 2 also caused the formation of equimolar amounts of ADP-ribose(P) and nicotinamide. Dose-dependent experiments, with increasing Fe 2+ iron (concentration range 3-180 μM) or H 2O 2 (concentration range 50-1000 μM), were carried out at pH 6.5 in 50 mM ammonium acetate. NAD(P) +, ADP-ribose(P) and nicotinamide formation increased by increasing the amount of hydroxyl radicals produced in the medium. Under such incubation conditions NAD(P) +/ADP-ribose(P) ratio was about 4 at any Fe 2+ or H 2O 2 concentration. By varying pH to 2.0, 3.0, 4.0, 4.5, 5.0, 5.5, 6.0, 7.0 and 7.4, NAD(P) +/ADP-ribose(P) ratio changed to 5.5, 3.2, 1.8, 1.6, 2.0, 2.5, 3.0, 5.4 and 6.5, respectively. Kinetic experiments indicated that 90-95% of all compounds were generated within 5s from the beginning of the Fenton reaction. Inhibition of ADP-ribose(P), nicotinamide and NAD(P) + production of Fe 2+-H 2O 2-treated NAD(P)H samples, was achieved by adding mannitol (10-50 mM) to the reaction mixture. Differently, selective and total inhibition of ADP-ribose(P) and nicotinamide formation was obtained by performing the Fenton reaction in an almost completely anhydrous medium, i.e. in HPLC-grade methanol. Experiments carried out in isolated postischemic rat hearts perfused with 50 mM mannitol, showed that, with respect to values of control hearts, this hydroxyl radical scavenger prevented reperfusion-associated pyridine coenzyme depletion and ADP-ribose formation. On the basis of these results, a possible mechanism of action of ADP-ribose(P) and nicotinamide generation through the interaction between NAD(P)H and hydroxyl radical (which does not involve the C-center where “conventional” oxidation occurs) is presented. The implication of this phenomenon in the pyridine coenzyme depletion observed in postischemic tissues is also discussed. 相似文献
12.
The effect of lactic acid (lactate) on Fenton based hydroxyl radical ( ·OH) production was studied by spin trapping, ESR, and fluorescence methods using DMPO and coumarin-3-carboxylic acid (3-CCA) as the ·OH traps respectively. The ·OH adduct formation was inhibited by lactate up to 0.4mM (lactate/iron stoichiometry = 2) in both experiments, but markedly enhanced with increasing concentrations of lactate above this critical concentration. When the H 2O 2 dependence was examined, the DMPO-OH signal was increased linearly with H 2O 2 concentration up to 1 mM and then saturated in the absence of lactate. In the presence of lactate, however, the DMPO-OH signal was increased further with higher H 2O 2 concentration than 1 mM, and the saturation level was also increased dependent on lactate concentration. Spectroscopic studies revealed that lactate forms a stable colored complex with Fe 3+ at lactate/Fe 3+ stoichiometry of 2, and the complex formation was strictly related to the DMPO-OH formation. The complex formation did not promote the H 2O 2 mediated Fe 3+ reduction. When the Fe 3+-lactate (1:2) complex was reacted with H 2O 2, the initial rate of hydroxylated 3-CCA formation was linearly increased with H 2O 2 concentrations. All the data obtained in the present experiments suggested that the Fe 3+-lactate (1:2) complex formed in the Fenton reaction system reacts directly with H 2O 2 to produce additional ·OH in the Fenton reaction by other mechanisms than lactate or lactate/Fe 3+ mediated promotion of Fe 3+/Fe 2+ redox cycling. 相似文献
13.
We sought to confirm a recent report that Fe +2 uptake into rat brush-border membrane vesicles is markedly increased by short-term consumption of iron-deficient diet, with no additional enhancement as the animal becomes functionally iron-deficient with continuing dietary Fe deprivation. In addition, we investigated whether previously observed in vivo absorption interactions of iron, zinc, and manganese occur in the brush border membrane vesicles uptake process, and whether short-term or long-term consumption of an iron-deficient diet affects the interaction at the uptake level. We did not observe any differences in Fe +2 uptake between normal and iron-deficient brush border membrane vesicles, even when the iron status contrast was intensified by feeding a high iron versus iron-deficient diet for 3 weeks. Equimolar Zn +2 and Mn +2 decreased Fe +2 uptake by 29 to 50% and 11 to 39%, respectively. Iron deficiency did not alter these effects. Equimolar Fe +2 decreased Zn +2 uptake by 13 to 22%. Calcium, included as a negative control, did not affect Fe +2 uptake. Thus, some competition between Fe +2 and similar divalent cations does occur at the level of the brush border membrane; the exact nature of this competition remains to be determined. 相似文献
14.
The reaction of Fe II oxalate with hydrogen peroxide and dioxygen was studed for oxalate concentrations up to 20 mM and pH 2-5, under which conditions mono- and bis-oxalate comlexes (Fe II(ox) and Fe II(ox) 22-) and uncomplexed Fe 2+ must be considered. The reaction of Fe II oxalate with hydrogen peroxide (Fe 2+ + H 2O 2 → Fe 3+ + *OH + OH -) was monitored in continuous flow by ESR with t-butanol as a radical trap. The reaction is much faster than for uncomplexed Fe 2+ and a rate constant, k = 1 × 10 4 M- 1 s -1 is deduced for Fe II(ox). The reaction of Fe II oxalate with dioxygen is strongly pH dependent in a manner which indicates that the reactive species is Fe II(ox) 22-, for which an apparent second order rate constant, k = 3.6 M -1 s -1, is deduced. Taken together, these results provide a mechanism for hydroxyl radical production in aqueous systems containing Fe II complexed by oxalate. Further ESR studies with DMPO as spin trap reveal that reaction of Fe II oxalate with hydrogen peroxide can also lead to formation of the carboxylate radical anion (CO 2*-), an assignment confirmed by photolysis of Fe III oxalate in the presence of DMPO. 相似文献
15.
We are addressing the puzzling metal ion specificity of Fe- and Mn-containing superoxide dismutases (SODs) [see C.K.Vance, A.-F. Miller, J. Am. Chem. Soc. 120(3) (1998) 461–467]. Here, we test the significance to activity and active site integrity of the Gln side chain at the center of the active site hydrogen bond network. We have generated a mutant of MnSOD with the active site Gln in the location characteristic of Fe-specific SODs. The active site is similar to that of MnSOD when Mn 2+, Fe 3+ or Fe 2+ are bound, based on EPR and NMR spectroscopy. However, the mutant’s Fe-supported activity is at least 7% that of FeSOD, in contrast to Fe(Mn)SOD, which has 0% of FeSOD’s activity. Thus, moving the active site Gln converts Mn-specific SOD into a cambialistic SOD and the Gln proves to be important but not the sole determinant of metal-ion specificity. Indeed, subtle differences in the spectra of Mn 2+, Fe 3+ and 1H in the presence of Fe 2+ distinguish the G77Q, Q146A mut-(Mn)SOD from WT (Mn)SOD, and may prove to be correlated with metal ion activity. We have directly observed the side chain of the active site Gln in Fe 2+SOD and Fe 2+(Mn)SOD by 15N NMR. The very different chemical shifts indicate that the active site Gln interacts differently with Fe 2+ in the two proteins. Since a shorter distance from Gln to Fe and stronger interaction with Fe correlate with a lower Em in Fe(Mn)SOD, Gln has the effect of destabilizing additional electron density on the metal ion. It may do this by stabilizing OH − coordinated to the metal ion. 相似文献
16.
Isolated plasma membranes of lactating mouse mammary gland were treated with different concentrations of ascorbate, sodium citrate, sodium bicarbonate, combinations of them (from 16 x 10 −10 to 4 x 10 −6 moles/L) and studied for the binding of 59Fe 2+ and 59Fe 3+ at pH 7.4. The results show that the Fe 3+ form of iron is under a greater influence of anions used in these experiments. The Fe 2+ form of iron is weakly bounded and affected. It is suggested that the form with a greater positive electric charge is more effectively bound to the receptors in plasma membranes. 相似文献
17.
The role of histidine on DNA breakage induced by hydrogen peroxide (H 2O 2) and ferric ions or by H 2O 2 and cupric ions was studied on purified DNA. L-histidine slightly reduced DNA breakage by H 2O 2 and Fe 3+ but greatly inhibited DNA breakage by H 2O 2 and Cu 2+. However, only when histidine was present, the addition of EDTA to H 2O 2 and Fe 3+ exhibited a bimodal dose response curve depending on the chelator metal ratio. The enhancing effect of histidine on the rate of DNA degradation by H 2O 2 was maximal at a chelator metal ratio between 0.2 and 0.5, and was specific for iron. When D-histidine replaced L-histidine, the same pattern of EDTA dose response curve was observed. Superoxide dismutase greatly inhibited the rate of DNA degradation induced by H 2O 2, Fe 3+, EDTA and L-histidine involving the superoxide radical.
These studies suggest that the enhancing effect of histidine on the rate of DNA degradation by H 2O 2 and Fe 3+ is mediated by an oxidant which could be a ferrous-dioxygen-ferric chelate complex or a chelate-ferryl ion. 相似文献
18.
In 1999, we first reported that a white rot fungus, Ceriporiopsis subvermispora produced a series of novel alkylitaconic acids (ceriporic acids). In the present paper we synthesized the metabolite, 1-nonadecene-2,3-dicarboxylic acid (ceriporic acid B) by Grignard reaction to analyze chemical properties of the alkylitaconates. Mass spectrometer (MS) and nuclear magnetic resonance (NMR) spectra of the synthetic compound was identical to those of the fungal metabolite isolated. The dicarboxylic acid inhibited autoxidation of Fe 2+ to Fe 3+ as well as reduction of Fe 3+ to Fe 2+ by the strong natural reductants, cysteine, glutathione, and ascorbic acid. The formation of charge transfer complexes (CTCs) between 1-heptadecene-2,3-dicarboxylic acid and oxidized intermediates from phenolic substrates were also observed. Thus, we herein report that the new class of lipid-related metabolites produced by C. subvermispora are potential metabolites participating in the control of iron redox reactions and CTCs formation from oxidized lignin fragments. 相似文献
19.
The authors previously reported that Fe 2+ is capable of increasing the binding of dopamine and of serotonin to “serotonin binding proteins” which are present in soluble extracts from calf brain. In this study, it is shown that Mn 2+ and Cu 2+ are also capable of increasing the binding, but for dopamine only. As for Fe 2+, Mn 2+ and Cu 2+ are likely to promote the binding by virtue of their ability to enhance the oxidation of dopamine into dopamine-O-quinone, a derivative which is known to undergo covalent association with sulfhydryl groups of proteins. Data such as the irreversible nature of the majority of the binding, the inhibitory action of reducing agents (sodium ascorbate) and of reagents which contain, or modify sulfhydryl groups (reduced glutathione) are compatible with such a mechanism. The three metal ions are also capable of inactivating part of the binding sites on SBP directly; this effect is more pronounced for Cu 2+ than for Fe 2+ and it is only weak for Mn 2+. The Fe 2+-mediated binding of dopamine is inhibited by the superoxide dismutase enzyme, and it was therefore suggested that Fe 2+ enhances the oxidation of dopamine by virtue of its ability to produce superoxide radicals out of dissolved molecular oxygen. Such a mechanism does not appear to take place in the case of Mn 2+ and Cu 2+. Instead, it is likely that Cu 2+ and dopamine form a complex which is highly susceptible towards oxidation by dissolved molecular oxygen. Mn 2+, on the other hand, can easily be oxidized into Mn 3+, which is capable to oxidize dopamine by itself. Chronic manganese intoxication (from exposure to manganese) and Wilson's disease (related to inadequate elimination of copper) go along with neurological symptoms which are very similar to those encountered in Parkinson's disease. Our data indicate that manganese and copper ions accelerate the oxidation of catecholamines to produce toxic quinones. These quinones could, at least in part, account for the degeneration of dopamininergic neurons in such pathologies. 相似文献
20.
Biosensors incorporating mammalian cells have a distinct advantage of responding in a manner which offers insight into the physiological effect of an analyte. To investigate the potential applications of cell-based biosensors on heavy metal toxicity detection, a novel biosensor for monitoring electrophysiological activity was developed by light-addressable potentiometric sensor (LAPS). Extracellular field potentials of spontaneously beating cardiomyocytes could be recorded by LAPS in the range of 20 μV to nearly 40 μV with frequency of 0.5–3 Hz. After exposed to different heavy metal ions (Hg 2+, Pb 2+, Cd 2+, Fe 3+, Cu 2+, Zn 2+; in concentration of 10 μM), cardiomyocytes demonstrated characteristic changes in terms of beating frequency, amplitude and duration under the different toxic effects of ions in less than 15 min. This study suggests that, with the physiological monitoring, it is possible to use the cardiac cell-based biosensor to study acute and eventually chronic toxicities induced by heavy metal ions in a long-term and no-invasive way. 相似文献
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