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1.
Copper-induced changes in the growth, oxidative metabolism, and saponin production in suspension culture roots of Panax ginseng in bioreactors 总被引:3,自引:0,他引:3
Roots of Panax ginseng exposed to various concentrations of Cu (0.0, 5, 10.0, 25.0, and 50.0 μM) accumulated high amounts of Cu in a concentration-dependent and duration-dependent manner. Roots treated with 50 μM Cu resulted in 52% and 89% growth inhibition after 20 and 40 days, respectively. Saponin synthesis was stimulated at a Cu concentration between 5 and 25 μM but decreased at 50 μM Cu. Malondialdehyde content (MDA), lipoxygenase activity (LOX), superoxide ion (O2
•−) accumulation, and H2O2 content at 5 and 10 μM Cu-treated roots were not increased but strongly increased at 50 μM Cu resulting in the oxidation of ascorbate (ASC) and glutathione (GSH) to dehydroascorbate (DHA) and glutathione disulfide (GSSG), respectively indicating a clear oxidative stress. Seven well-resolved bands of superoxide dismutase (SOD) were detected in the gel and an increase in SOD activity seemed to be mainly due to the induction of Fe-SOD 3. Five to 10 μM Cu slightly induced activity of ascorbate peroxidase (APX) and dehydroascorbate reductase (DHAR), guaiacol peroxidase (G-POD) but inhibited monodehydroascorbate reductase (MDHAR) and glutathione reductase (GR) enzyme activities. No changes in catalase (CAT) activity and in activity gel were found up to 25 μM Cu, but both G-POD and CAT activities were inhibited at 50 μM Cu. Glutathione metabolism enzymes such as γ-glutamylcysteine synthetase (γ-GCS), glutathione-S-transferase (GST), and glutathione peroxidase activities (GPx) were activated at 5 and 10 μM Cu but were strongly inhibited at 50 μM Cu due to the Cu accumulation in root tissues. The strong depletion of GSH at 50 μM Cu was associated to the strong induction of γ-glutamyltranspeptidase (γ-GGT) activity. These results indicate that plant could grow under Cu stress (5–25 μM) by modulating the antioxidant defense mechanism for combating Cu induced oxidative stress. 相似文献
2.
The effect of zinc on various pulmonary cell lines has been studied by measuring the depletion of total cellular glutathione
after exposure to zinc(II) chloride at different concentrations.
Total cellular glutathione (cGS) was measured at 31 ± 3 nmol/mg, 3.8 ± 0.6 nmol/mg, and 3.7 ±1.2 nmol/mg protein in A549,
L2, and 11Lu cells, respectively. After treatment with buthionine sulfoximine (BSO), the cGS levels decreased by 20% in A549
cells and below 0.2 nmol/mg in L2 and 11Lu cells.
Exposure of A549 cells to 25–200 μM ZnCl2 for 4 h alone decreased the cGS content to 60–80%. There was little additional effect in BSO-pretreated cells. In L2 and
11Lu cells, the decrease of cGS was 70–85% following exposure to 15–150 μM ZnCl2 for 2 h. If BSO was also used, the decrease in cGS was 85–95% in L2 cells and 75–85% in 11Lu cells.
Exposure to 25–250 μM ZnCl2 for 2 h diminished protein synthesis as determined by radiolabeled methionine incorporation, with half-maximum inhibition
(EC50) from 40–160 μM ZnCl2. To attain similar EC50 values in BSO-pretreated cells, only about half the zinc concentrations were required as compared to cells without pretreatment.
The decrease of cGS was accompanied by an increased ratio of oxidized : reduced glutathione that was more pronounced in cells
with low glutathione content. 相似文献
3.
Karl-Ernst Kaissling 《Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology》2009,195(10):895-922
Modelling reveals that within about 3 ms after entering the sensillum lymph, 17% of total pheromone is enzymatically degraded
while 83% is bound to the pheromone-binding protein (PBP) and thereby largely protected from enzymatic degradation. The latter
proceeds within minutes, 20,000-fold more slowly than with the free pheromone. In vivo the complex pheromone–PBP interacts
with the receptor molecule. At weak stimulation the half-life of the active complex is 0.8 s due to the postulated pheromone
deactivation. Most likely this process is enzymatically catalysed; it changes the PBP into a scavenger form, possibly by interference
with the C-terminus. The indirectly determined PBP concentration (3.8 mM) is close to direct measurements. The calculated
density of receptor molecules within the plasma membrane of the receptor neuron reaches up to 6,000 units per μm2. This is compared with the estimated densities of the sensory-neuron membrane protein and of ion channels. The EC50 of the model pheromone–PBP complex interacting with the receptor molecules is 6.8 μM, as compared with the EC50 = 1.5 μM of bombykol recently determined using heterologous expression. A possible mechanism widening the range of stimulus
intensities covered by the dose–response curve of the receptor-potential is proposed. 相似文献
4.
Andrea Ferrigno Cesarina Gregotti Plinio Richelmi Mariapia Vairetti 《In vitro cellular & developmental biology. Animal》2010,46(5):445-449
In the present study, the effects of dexamethasone on cadmium-induced toxicity were evaluated in isolated rat hepatocytes.
Hepatocytes were cultured for 24 h in William’s E medium containing fetal calf serum (10%), insulin (0.1 IU/ml), and glucagon
(0.01 μM) in the absence or presence of 0.1 μM dexamethasone. Cadmium chloride, 5 or 10 μM, was added to the medium and the
toxicity was evaluated for up to 48 h after treatment. Lactate dehydrogenase (LDH) release, the reduced and oxidized glutathione
ratio (GSH/GSSG), protein-SH groups, and lipid peroxidation levels were evaluated. Cadmium induced a dose- and time-dependent
LDH release in control hepatocytes at 24 h (Cd 10 μM 42%) while hepatocytes pretreated with dexamethasone showed lower necrosis
(Cd 10 μM 12% at 24 h). GSH/GSSH ratio and protein-SH groups were higher while lipid peroxidation was lower in dexamethasone-treated
hepatocytes as compared with untreated cells. In conclusion, cadmium toxicity was associated with an increase in intracellular
oxidative stress responsible for accelerated cell death. The use of dexamethasone prevented cadmium damage, suggesting that
the cytoprotective action of this hormone is related to its effect in preventing changes in thiols such as glutathione and
protein-SH groups. 相似文献
5.
Malin H. Stridh Fernando Correa Christina Nodin Stephen G. Weber Fredrik Blomstrand Michael Nilsson Mats Sandberg 《Neurochemical research》2010,35(8):1231-1238
Efflux of glutathione (GSH) from astrocytes has been suggested as a key factor for neuroprotection by astrocytes. Here we
evaluated if the Nrf2 activator curcumin affects basal and stimulated (Ca2+ omission) GSH efflux from cultures of astroglial cells. Stimulated efflux of GSH was observed at medium concentration of
0, 0.1 mM Ca2+, but not at 0.2 or 0.3 mM Ca2+. Astroglia treated with 30 μM curcumin increased the cellular content of GSH in parallel with elevated basal and stimulated
efflux. Conversely treatment with buthionine sulfoximine lowered efflux of GSH. The efflux stimulated by Ca2+- omission was not affected by the P2X7-receptor antagonist Blue Brilliant G (100 nM) or the pannexin mimetic/blocking peptide
10Panx1 but inhibited by the gap junction blocker carbenoxolone (100 μM) and a hemichannel blocker Gap26 (300 μM). RNAi directed
against Nrf2 partly inhibited the effect of curcumin. The results show that elevated cellular GSH by curcumin treatment enhance
efflux from astroglial cells, a process which appear to be a prerequisite for astroglial mediated neuroprotection. 相似文献
6.
Martin Bačkor Barbara Pawlik-Skowrońska Jana Bud’ová Tadeusz Skowroński 《Plant Growth Regulation》2007,52(1):17-27
Cysteine, glutathione (GSH) and phytochelatins were determined in the cells of both wild and copper tolerant strains of the
lichen alga Trebouxia erici following short-term (24 h) exposure to copper and cadmium and long-term (4 weeks) exposure to copper. Both metals caused
concentration dependent synthesis of phytochelatins (PC2–PC5), but cadmium was a more potent activator of phytochelatin synthesis, even inducing synthesis of PC5. The copper-tolerant strain did not reveal a higher degree of phytochelatin synthesis than the wild strain, and at 5 μM Cu
production of phytochelatins was in fact significantly lower. Lower levels of phytochelatin correlated with significantly
decreased intracellular copper content in the copper-tolerant strain. Both strains maintained high GSH levels even at a high
copper concentration of 5 μM, and only the highest copper concentration (10 μM) was toxic for both strains, causing a decrease
of GSH and PC content in algal cells. Cadmium had less effect on GSH in the cells of both tested strains. In the long term
experiments, only relatively small amounts of PC2 were detected in both strains, but the copper-tolerant strain retained significantly higher levels of reduced glutathione,
probably due to the lesser degree of oxidative stress caused by Cu. The significant increase of cysteine synthesis in the
copper-tolerant strain found in the present study may be related to copper tolerance in T. erici, while decreased intracellular Cu uptake, detoxification by PCs and increased free proline levels for protection of chloroplast
membranes may also be implicated. 相似文献
7.
The role of glutathione (GSH) in the adaptation of wild type Arabidopsis thaliana plants to Cd stress was investigated. The nutrient solution (control or containing 50 or 100 μM Cd) was supplemented with
buthionine sulfoximine (BSO; 50, 100, 500 μM, to decrease the GSH content in plants) or GSH (50, 100, 500 μM, to increase
its content in plants) in order to find how GSH content could regulate Cd stress responses. BSO application did not influence
plant biomass, while exogenous GSH (especially 500 μM) reduced root biomass. BSO (500μM) in combination with Cd (100 μM) increased
Cd toxicity on root growth (by over 50 %), most probably due to reduced GSH content and phytochelatin (PC) accumulation (by
over 96 %). On the other hand, combination of exogenous GSH (500 μM) with Cd (100 μM) was also more toxic to plants than Cd
alone despite a significant increase in GSH and PC accumulation (up to 2.7 fold in the roots). This fact could indicate that
the natural content of endogenous GSH in wild type A. thaliana plants is sufficient for Cd-tolerance. A decrease in this GSH content led to decreased Cd-tolerance of the plants but an
increase in GSH content did not enhance Cd-tolerance, and it showed even toxic effect on the plants. 相似文献
8.
The protein bCblC (bCblCpro) is a bovine homolog of a human B12 trafficking chaperone that is responsible for the processing of vitamin B12 and its escorted delivery in intracellular B12 metabolism. In this study, we found that bCblCpro is highly thermolabile with a T
m = 42.0 ± 0.2 °C as shown for the human homolog, suggesting thermal regulation of these proteins. Binding of the reduced form
of glutathione (GSH) that is a predominant cellular thiol increased the T
m of bCblCpro from 42 °C to ~45 °C (ΔT
m max = 3.1 ± 0.2 °C and AC50 = 2.1 ± 0.5 mM). Binding of vitamin B12 and its derivatives also stabilized bCblCpro increasing the T
m to a different extent and vitamin B12 (cyanocobalamin, CNCbl) was the least efficient (ΔT
m max = 4.3 ± 0.3 °C and AC50 = 291 ± 36 μM). However, the stabilizing effect of CNCbl was significantly greater for GSH-bound bCblCpro (ΔT
m max = 12.8 ± 0.6 °C and AC50 = 9.3 ± 1.6 μM) than for GSH-free bCblCpro. In addition, the stabilizing effect of GSH was also greater for CNCbl-bound bCblCpro
(ΔT
m max = 9.3 ± 0.3 °C and AC50 = 57.0 ± 6.8 μM). Limited proteolysis revealed that thermal stabilization of bCblCpro is derived from conformational changes
of the protein induced by binding of the ligands. The results in this study indicate that GSH cooperates with vitamin B12 in thermal stabilization of bCblCpro and is a positive regulator of the protein. 相似文献
9.
Use of oxygenates in gasoline in the United States may increase atmospheric levels of aldehydes. To assist in health assessments of inhalation exposure to aldehydes, we studied glutathione (GSH) depletion by low-molecular-weight n-alkanals and 2-alkenals, ubiquitous air pollutants, in adult rat lung (ARL) cells by laser cytometry. For each homologous series, the effective aldehyde concentration that depleted GSH by 50% (EC50) in ARL cells correlates with published values for the median lethal dose of the chemicals and with Hammett/Taft electronic parameters, * for n-alkanals and p* for 2-alkenals. n-Alkanals (EC50, 110–400 mmol/L) were 1000 times less effective in depleting GSH than were 2-alkenals (EC50, 2–180 mol/L), of which acrolein was the most potent. Ability of the 2-alkenals to deplete GSH follows the second-order rate constant for adduct formation. Ability of n-alkanals to deplete GSH follows chain length. Within a homologous series of low-molecular-weight aldehydes, structure–activity relationships are useful for predicting the toxicity of the aldehydes in vitro and in vivo. 相似文献
10.
Greenhouse hydroponic experiments were conducted using Cd-sensitive (Xiushui63) and tolerant (Bing97252) rice genotypes to
evaluate genotypic differences in response of photosynthesis and phytochelatins to Cd toxicity in the presence of exogenous
glutathione (GSH). Plant height, chlorophyll content, net photosynthetic rate (Pn), and biomass decreased in 5 and 50 μM Cd
treatments, and Cd-sensitive genotype showed more severe reduction than the tolerant one. Cadmium stress caused decrease in
maximal photochemical efficiency of PSII (Fv/Fm) and effective PSII quantum yield [Y(II)] and increase in quantum yield of
regulated energy dissipation [Y(NPQ)], with changes in Cd-sensitive genotype being more evident. Cadmium-induced phytochelatins
(PCs), GSH, and cysteine accumulation was observed in roots of both genotypes, with markedly higher level in PCs and GSH on
day 5 in Bing97252 compared with that measured in Xiushui63. Exogenous GSH significantly alleviated growth inhibition in Xiushui63
under 5 μM Cd and in both genotypes in 50 μM Cd. External GSH significantly increased chlorophyll content, Pn, Fv/Fm, and
Y(II) of plants exposed to Cd, but decreased Y(NPQ) and the coefficient of non-photochemical quenching (qN). GSH addition
significantly increased root GSH content in plants under Cd exposure (except day 5 of 50 μM Cd) and induced up-regulation
in PCs of 5 μM-Cd-treated Bing97252 throughout the 15-day and Xiushui63 of 5-day exposure. The results suggest that genotypic
difference in the tolerance to Cd stress was positively linked to the capacity in elevation of GSH and PCs, and that alleviation
of Cd toxicity by GSH is related to significant improvement in chlorophyll content, photosynthetic performance, and root GSH
levels. 相似文献
11.
Selvatici R Previati M Marino S Marani L Falzarano S Lanzoni I Siniscalchi A 《Neurochemical research》2009,34(5):909-916
The features of neuronal damage induced by the mitochondrial toxin NaN3 were investigated in rat primary cortical neuron cultures. Cell viability (MTT colorimetric determination) and transmembrane
mitochondrial potential (J-C1 fluorescence) were concentration-dependently reduced 24 h after NaN3; neither nuclear fragmentation by DAPI, nor Annexin V positivity by flow cytometry were detected, ruling out the occurrence
of apoptosis. The loss in cell viability (to 54 ± 2%) observed 24 h after a 10-min treatment with 3 mM NaN3 was prevented by the NMDA glutamate receptor antagonist MK801 (1 μM), by the antioxidants trolox (100 μM) and acetyl-l-carnitine (1 mM) and by the nitric oxide synthase inhibitor, L-NAME (100 μM), but not by the guanylylcyclase inhibitor ODQ,
10 μM. The mitochondrial dysfunction induced by NaN3 provides a common platform for investigating the mechanisms of both ischemic and degenerative neuronal injury, useful for
screening potential protective agents against neuronal death.
Rita Selvatici and Maurizio Previati equally contributed to the work. 相似文献
12.
Wormser C Pore SA Elperin AB Silverman LN Light DB 《The Journal of membrane biology》2011,242(2):75-87
This study examined the role of a P2 receptor and arachidonic acid (AA) in regulatory volume decrease (RVD) by American alligator
red blood cells (RBCs). Osmotic fragility was determined optically, mean cell volume was measured by electronic sizing, and
changes in intracellular Ca2+ concentration were visualized using fluorescence microscopy. Gadolinium (50 μM), hexokinase (2.5 U/ml), and suramin (100 μM)
increased osmotic fragility, blocked volume recovery after hypotonic shock, and prevented a rise in intracellular Ca2+ that normally occurs during cell swelling. The P2X antagonists PPADS (50 μM) and TNP-ATP (10 μM) also increased fragility
and inhibited volume recovery. In contrast, ATPγS (10 μM), α,β-methylene-ATP (50 μM) and Bz-ATP (50 μM) had the opposite effect,
whereas 2-methylthio-ATP (50 μM) and UTP (10 μM) had no effect. In addition, the phospholipase A2 (PLA2) inhibitors ONO-RS-082 (10 μM), chlorpromazine (10 μM), and isotetrandrine (10 μM) increased osmotic fragility and blocked
volume recovery, whereas AA (10 μM) and its nonhydrolyzable analog eicosatetraynoic acid (ETYA, 10 μM) had the reverse effect.
Further, AA (10 μM), but not ATPγS (10 μM), prevented the inhibitory effect of a low Ca2+-EGTA Ringer on RVD, whereas both AA (10 μM) and ATPγS (10 μM) caused cell shrinkage under isosmotic conditions. In conclusion,
our results are consistent with the presence of a P2-like receptor whose activation stimulated RVD. In addition, AA also was
important for volume recovery. 相似文献
13.
In this study, the effect of cadmium (Cd) on cell viability and its accumulation in Bradyrhizobium spp. (peanut microsymbionts) as well as the role of glutathione (GSH) in the tolerance to this metal were investigated. A
reference strain recommended as peanut inoculant (Bradyrhizobium sp. SEMIA6144) grew up to 10 μM Cd meanwhile a GSH-deficient mutant strain (Bradyrhizobium sp. SEMIA6144-S7Z) was unable to grow at this concentration. Two native peanut isolates obtained from Córdoba soils (Bradyrhizobium sp. NLH25 and Bradyrhizobium sp. NOD31) tolerated up to 30 μM Cd. The analysis of Cd content showed that Bradyrhizobium sp. SEMIA6144 accumulated a high amount of this metal, but a considerable inhibition of growth was observed compared to tolerant
strains at 10 μM Cd. At this concentration, the intracellular GSH content of all the Bradyrhizobium sp. strains was not modified in comparison to control conditions. However, at 30 μM Cd, the intracellular GSH content significantly
increased in Bradyrhizobium sp. strains NLH25 and NOD31. Thus, the distinct response of each Bradyrhizobium sp. strain to Cd reveals that, even in closely related lineages, there are strain-specific variations influencing the levels
of tolerance to this metal. Indeed, the native peanut isolates tolerated higher Cd concentration than the reference strain,
possibly due to an increase in GSH levels which could act as a detoxifying agent. 相似文献
14.
It is well known that antioxidants containing sulfhydryl (−SH) groups are protective against the toxic effects of mercury.
The current study was designed to elucidate the mechanism(s) of the cytoprotective effects of glutathione (GSH) and N-acetylcysteine (NAC) against the toxicity of inorganic mercury (HgCl2) in neuroblastoma cells (N-2A). The obtained results demonstrated the protective effects of these compounds in a dose dependant
manner up to 95 and 74% cell viability, respectively as compared to the control of HgCl2 of 10%. The administration of buthionine sulfoximine (BSO), an inhibitor of GSH synthesis, increased the toxicity of HgCl2 in a dose dependent manner. Moreover, BSO treatment attenuated the levels of the cellular free −SH concentrations at low
concentrations (1–100 μM) of HgCl2. The data also show that cellular thiol concentrations were augmented in the presence of GSH and NAC and these compounds
were cytoprotective against HgCl2 and this is due to up regulating of GSH synthesis. A reduction in intracellular levels of GSH was observed with treatment
of HgCl2. In addition, the ratio of GSH/GSSG increased from 16:1 to 50:1 from 1 to 10 μM concentration of HgCl2. The ratio of GSH/GSSG then decreased from 4:1 to 0.5:1 with the increase of concentration of HgCl2 between 100 μM and 1 mM due to the collapse of the N-2A cells. It was of interest to note that the synthesis of GSH was stimulated
in cells exposed to low concentration of HgCl2 when extra GSH is available. These data support the idea that the loss of GSH plays a contributing role to the toxic effects
of HgCl2 and that inorganic mercury adversely affects viability, through altering intracellular −SH concentrations. The data further
indicate that the availability of GSH to the cells may not be sufficient to provide protection against mercury toxicity and
the de novo synthesis of intracellular GSH is required to prevent the damaging effects of mercury. 相似文献
15.
The effects of arsenite treatment on generation of reactive oxygen species, induction of oxidative stress, response of antioxidative
system, and synthesis of phytochelatins were investigated in two indica rice (Oryza sativa L.) cvs. Malviya-36 and Pant-12 grown in sand cultures for a period of 5–20 days. Arsenite (As2O3; 25 and 50 μM) treatment resulted in increased formation of superoxide anion (O2.−), elevated levels of H2O2 and thiobarbituric acid reactive substances, showing enhanced lipid peroxidation. An enhanced level of ascorbate (AA) and
glutathione (GSH) was observed irrespective of the variation in the level of dehydroascorbate (DHA) and oxidized glutathione
(GSSG) which in turn influenced redox ratios AA/DHA and GSH/GSSG. With progressive arsenite treatment, synthesis of total
acid soluble thiols and phytochelatins (PC) increased in the seedlings. Among antioxidative enzymes, the activities of superoxide
dismutase (EC 1.15.1.1), catalase (EC 1.11.1.6), total ascorbate peroxidase (APX, EC 1.11.1.11), chloroplastic ascorbate peroxidase,
guaiacol peroxidase (EC 1.11.1.7), monodehydroascorbate reductase (EC 1.6.5.4), and glutathione reductase (EC 1.6.4.2) increased
in arsenite treated seedlings, while dehyroascorbate reductase (EC 1.8.5.1) activity declined initially during 5–10 days and
increased thereafter. Results suggest that arsenite treatment causes oxidative stress in rice seedlings, increases the levels
of many enzymatic and non-enzymatic antioxidants, and induces synthesis of thiols and PCs, which may serve as important components
in mitigating arsenite-induced oxidative damage. 相似文献
16.
Dopamine auto-oxidation and the consequent formation of reactive oxygen species and electrophilic quinone molecules have been
implicated in dopaminergic neuronal cell death in Parkinson’s disease. We reported here that in PC12 dopaminergic neuronal
cells dopamine at noncytotoxic concentrations (50–150 μM) potently induced cellular glutathione (GSH) and the phase 2 enzyme
NAD(P)H:quinone oxidoreductase 1 (NQO1), two critical cellular defenses in detoxification of ROS and electrophilic quinone
molecules. Incubation of PC12 cells with dopamine also led to a marked increase in the mRNA levels for γ-glutamylcysteine
ligase catalytic subunit (GCLC) and NQO1. In addition, treatment of PC12 cells with dopamine resulted in a significant elevation
of GSH content in the mitochondrial compartment. To determine whether treatment with dopamine at noncytotoxic concentrations,
which upregulated the cellular defenses could protect the neuronal cells against subsequent lethal oxidative and electrophilic
injury, PC12 cells were pretreated with dopamine (150 μM) for 24 h and then exposed to various cytotoxic concentrations of
dopamine or 6-hydroxydopamine (6-OHDA). We found that pretreatment of PC12 cells with dopamine at a noncytotoxic concentration
led to a remarkable protection against cytotoxicity caused by dopamine or 6-OHDA at lethal concentrations, as detected by
3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium reduction assay. In view of the critical roles of GSH and NQO1 in protecting
against dopaminergic neuron degeneration, the above findings implicate that upregulation of both GSH and NQO1 by dopamine
at noncytotoxic concentrations may serve as an important adaptive mechanism for dopaminergic neuroprotection. 相似文献
17.
Uranium (U) as a redox-active heavy metal can cause various redox imbalances in plant cells. Measurements of the cellular
glutathione/glutathione disulfide (GSH/GSSG) by HPLC after cellular U contact revealed an interference with this essential
redox couple. The GSH content remained unaffected by 10 μM U whereas the GSSG level immediately increased. In contrast, higher
U concentrations (50 μM) drastically raised both forms. Using the Nernst equation, it was possible to calculate the half-cell
reduction potential of 2GSH/GSSG. In case of lower U contents the cellular redox environment shifted towards more oxidizing
conditions whereas the opposite effect was obtained by higher U contents. This indicates that U contact causes a consumption
of reduced redox equivalents. Artificial depletion of GSH by chlorodinitrobenzene and measuring the cellular reducing capacity
by tetrazolium salt reduction underlined the strong requirement of reduced redox equivalents. An additional element of cellular
U detoxification mechanisms is the complex formation between the heavy metal and carboxylic functionalities of GSH. Because
two GSH molecules catalyze electron transfers each with one electron forming a dimer (GSSG) two UO2
2+ are reduced to each UO2
+ by unbound redox sensitive sulfhydryl moieties. UO2
+ subsequently disproportionates to UO2
2+ and U4+. This explains that in vitro experiments revealed a reduction to U(IV) of only around 33% of initial U(VI). Cellular U(IV)
was transiently detected with the highest level after 2 h of U contact. Hence, it can be proposed that these reducing processes
are an important element of defense reactions induced by this heavy metal. 相似文献
18.
Summary. The neurotoxicity of domoic acid was studied in 2–3 week old rat hippocampal slice cultures, derived from 7 day old rat pups.
Domoic acid 0.1–100 μM was added to the culture medium for 48 hrs, alone or together with the glutamate receptor antagonists NS-102 (5-Nitro-6,7,8,9-tetrahydrobenzo[G]indole-2,3-dione-3-oxime),
NBQX (2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo(F)quinoxaline) or MK-801 ((+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10-imine
hydrogen maleate), followed by transfer of the cultures to normal medium for additional 48 hrs. Neuronal degeneration in the
fascia dentata (FD), CA3 and CA1 hippocampal subfields was monitored and EC50 values estimated by densitometric measurements of the cellular uptake of propidium iodide (PI). The CA1 region was most sensitive
to domoic acid, with an EC50 value of 6 μM domoic acid, estimated from the PI-uptake at 72 hrs. Protective effects of 10 μM NBQX against 3 and 10 μM domoic acid were observed for both dentate granule cells and CA1 and CA3c pyramidal cells. NS102 and MK 801 only displayed
protective effects when combined with NBQX. MK801 significantly increased the combined neuroprotective effect of NBQX and
NS102 against 10 μM domoic acid in both CA1 and FD, but not in CA3. We conclude, that domoic acid neurotoxicity in CA3 and in hippocampal slice
cultures in general primarily involves AMPA/kainate receptors. At high concentrations (10 μM domic acid) NMDA receptors are, however, also involved in the toxicity in CA1 and FD.
Received June 29, 2001 Accepted August 6, 2001 Published online June 3, 2002 相似文献
19.
Priyanka Srivastava Naresh Kasoju Utpal Bora Rakhi Chaturvedi 《Plant Cell, Tissue and Organ Culture》2009,99(1):1-7
Several secondary metabolites are present in Lantana camara L. as its leaves serve as reservoirs for various bioactive compounds. Callus cultures of L. camara were induced from leaf discs incubated on Murashige and Skoog medium supplemented with 5 μM 6-benzyladenine, 1 μM 2,4-dichlorophenoxyacetic
acid, and 1 μM α-naphthalene acetic acid (NAA). An aqueous extract (0.23%), obtained from these calli (50 g dry mass), had
an apparent cytotoxic effect on HeLa cells with an IC50 value of 1,500 μg/ml in 36 h. A dose-time dependent activity of the extract was established wherein higher dosage exhibited
increased activity; however, over time cell necrosis was observed. 相似文献
20.
Cell suspension cultures of red spruce (Picea rubens Sarg.) were selected to study the effects of cadmium (Cd) and zinc (Zn) on phytochelatins (PCs) and related metabolites after
24 h exposure. The PC2 and its precursor, γ-glutamylcysteine (γ-EC) increased two to fourfold with Cd concentrations ranging from 12.5 to 200 μM
as compared to the control. However, Zn-treated cells showed a less than twofold increase in γ-EC and PC2 levels as compared to the control even at the highest concentration of 800 μM. In addition, unidentified higher chain PCs
were also found in both the Cd and Zn treated cells and they increased significantly with increasing concentrations of Cd
and Zn. The cellular ratio of PC2 : Cd or Zn content clearly indicated that Cd (with ratios ranging from 0.131 to 0.546) is a more effective inducer of PC2 synthesis/accumulation than Zn (with ratios ranging from 0.032 to 0.102) in red spruce cells. A marginal decrease in glutathione
(GSH) was observed in both Cd and Zn treated cells. However, the GSH precursor, cysteine, declined twofold with all Cd concentrations
while the decrease with Zn was 1.5–2-fold only at the higher treatment concentrations of Zn as compared to control. In addition,
changes in other free amino acids, polyamines, and inorganic ions were also studied. These results suggest that PCs and their
biosynthetic intermediates play a significant role in red spruce cells protecting against Cd and Zn toxicity. 相似文献