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1.
Reactive oxygen species (ROS) released from polymorphonuclear leukocytes and macrophages could cause DNA damage, but also induce cell death. Therefore inhibition of cell death must be an important issue for accumulation of genetic changes in lymphoid cells in inflammatory foci. Scavengers in the post culture medium of four lymphoid cell lines, lymphoblastoid cell lines (LCL), Raji, BJAB and Jurkat cells, were examined. Over 80% of cultured cells showed cell death 24 h after xanthine (X)/xanthine oxidase (XOD) treatment, which was suppressed by addition of post culture medium from four cell lines in a dose-dependent manner. H 2O 2 but not O ·-2 produced by the X/XOD reaction was responsible for the cytotoxity, thus we used H 2O 2 as ROS stress thereafter. The H 2O 2-scavenging activity of post culture media from four cell lines increased rapidly at the first day and continued to increase in the following 2–3 days for LCL, Raji and BJAB cells. The scavenging substance was shown to be pyruvate, with various concentrations in the cultured medium among cell lines. Over 99% of total pyruvate was present in the extracellular media and less than 1% in cells. α-Cyano-4-hydroxycinnamate, a specific inhibitor of the H +-monocarbohydrate transporter, increased the H 2O 2-scavenging activity in the media from all four cell lines via inhibition of pyruvate re-uptake by cultured cells from the media. These findings suggest that lymphoid cells in inflammatory foci could survive even under ROS by producing pyruvate, so that accumulation of lymphoid cells with DNA damage is possible. 相似文献
2.
We previously reported that autophagy is upregulated in Prnp-deficient ( Prnp0/0) hippocampal neuronal cells in comparison to cellular prion protein (PrP C)-expressing ( Prnp+/+) control cells under conditions of serum deprivation. In this study, we determined whether a protective mechanism of PrP C is associated with autophagy using Prnp0/0 hippocampal neuronal cells under hydrogen peroxide (H 2O 2)-induced oxidative stress. We found that Prnp0/0 cells were more susceptible to oxidative stress than Prnp+/+ cells in a dose- and time-dependent manner. In addition, we observed enhanced autophagy by immunoblotting, which detected the conversion of microtubule-associated protein 1 light chain 3 β (LC3B)-I to LC3B-II, and we observed increased punctate LC3B immunostaining in H 2O 2-treated Prnp0/0 cells compared with H 2O 2-treated control cells. Interestingly, this enhanced autophagy was due to impaired autophagic flux in the H 2O 2-treated Prnp0/0 cells, while the H 2O 2-treated Prnp+/+ cells showed enhanced autophagic flux. Furthermore, caspase-dependent and independent apoptosis was observed when both cell lines were exposed to H 2O 2. Moreover, the inhibition of autophagosome formation by Atg7 siRNA revealed that increased autophagic flux in Prnp+/+ cells contributes to the prosurvival effect of autophagy against H 2O 2 cytotoxicity. Taken together, our results provide the first experimental evidence that the deficiency of PrP C may impair autophagic flux via H 2O 2-induced oxidative stress. 相似文献
4.
This study was carried out to evaluate the neuroprotective activity of polysaccharide extracts isolated from Perilla frutescens (PEPF) in H 2O 2-treated HT22 hippocampus cells. The PEPF treatment was found to increase the anti-oxidant activities of HT22 hippocampus cells. PEPF treatment resulted in a significant protection of HT22 hippocampus cells against H 2O 2-induced neurotoxicity, this protection ultimately occurred through an inhibition of ROS-mediated intracellular Ca 2+ levels leading to MAPKs and NF-κB, as well as the accumulation of PI3K/AKT and Nrf2-mediated HO-1/NQO1 pathways. Furthermore, PEPF not only decreased the expression of Bax, cytochrome c, and cleaved caspases-3, -8, and -9, but also increased the expression of PARP and Bcl-2 in the H 2O 2-treated HT22 hippocampus cells, which overall contributed to the neuroprotective action. PEPF retains its mitochondrial membrane potential and reduces the elevated levels of sub-G1 phase and apoptotic morphological features induced by H 2O 2. It also reduces the malondialdehyde levels and enhances the intracellular SOD activity. 相似文献
5.
A novel amperometric biosensor for xanthine was developed based on covalent immobilization of crude xanthine oxidase (XOD) extracted from bovine milk onto a hybrid nanocomposite film via glutaraldehyde. Toward the preparation of the film, a stable colloids solution of core–shell Fe 3O 4/polyaniline nanoparticles (PANI/Fe 3O 4 NPs) was dispersed in solution containing chitosan (CHT) and H 2PtCl 6 and electrodeposited over the surface of a carbon paste electrode (CPE) in one step. Scanning electron microscopy (SEM), Fourier transform infrared (FTIR) spectrophotometry, cyclic voltammetry (CV), and electrochemical impedance spectroscopy (EIS) were used for characterization of the electrode surface. The developed biosensor (XOD/CHT/Pt NPs/PANI/Fe 3O 4/CPE) was employed for determination of xanthine based on amperometric detection of hydrogen peroxide (H 2O 2) reduction at –0.35 V (vs. Ag/AgCl). The biosensor exhibited a fast response time to xanthine within 8 s and a linear working concentration range from 0.2 to 36.0 μM ( R2 = 0.997) with a detection limit of 0.1 μM (signal/noise [S/N] = 3). The sensitivity of the biosensor was 13.58 μA μM −1 cm −2. The apparent Michaelis–Menten ( Km) value for xanthine was found to be 4.7 μM. The fabricated biosensor was successfully applied for measurement of fish and chicken meat freshness, which was in agreement with the standard method at the 95% confidence level. 相似文献
6.
Summary L5178Y-R (LY-R) and L5178Y-S (LY-S) cells, differing in radiation sensitivity and susceptibility to the radiosensitizing effect of benzamide (Bz) were examined for susceptibility to hydrogen peroxide. Survival and chromatid aberration frequency indicated that LY-R cells were considerably more sensitive to H 2O 2 than LY-S cells. So, LY strains were found to be inversely crosssensitive to X/ rays and H 2O 2. The relative resistance to H 2O 2 corresponded with the previously found twofold difference in catalase activity (Jaworska et al. 1987). At higher concentrations H 2O 2 treatment caused interphase death, that was delayed by benzamide (Bz, 2 m M), an inhibitor of po1y(ADP-ribosylation), to a lesser extent in the more resistant cell subline (LY-S). From the examination of the H 2O 2 induced increase in the free Ca 2+ concentration (with or without 2 m M Bz treatment) with the use of Fura-2 it followed, that the cells responded to the oxidative stress by Ca 2+ release. The Ca 2+ concentration increase was neither directly related to the killing effect of H 2O 2 treatment, nor did it correspond with the twofold difference in catalase activity in LY strains. 相似文献
7.
The activity of 1-aminocyclopropane-1-carboxylic acid synthase (ACC synthase, ACS) and the concentrations of superoxide radical
(O 2−.) and hydrogen peroxide (H 2O 2) were measured in etiolated mungbean seedlings following their transfer to a growth chamber at 25°C after a 5-h-chilling
treatment at 5°C. All of these variables increased dramatically after the transfer, and strong correlations were found between
ACS activity and the concentrations of superoxide and H 2O 2. Exogenous applications of two generators of superoxide radicals, methylviologen (MV) and xanthine–xanthine oxidase (X–XOD),
enhanced ACS activity in seedlings, but their effects were inhibited by exogenous applications of specific scavengers of O 2−.. However, applications of H 2O 2 or specific H 2O 2-scavengers had no significant effects on seedlings ACS activity. The results indicate that O 2−. was involved in the chilling-induced increases in ACS activity, but not H 2O 2. ACS activity peaked ca. 8 h after the transfer, and then declined, but the decline could be counteracted by exogenous applications
of specific O 2−. scavengers, this suggests that damage was caused by superoxide radicals influencing ACS activity in etiolated mungbean seedlings.
Further analysis of changes in two key kinetic parameters of ACS activity— V
max (maximum velocity) and K
m (the Michaelis constant)—in the seedlings indicated that the presence of O 2−. may reduce K
m, i.e. increase substrate (S-adenosyl methionine, SAM) affinity. That would be the main mechanism responsible for the observed
chilling-induced increases in ACS activity in etiolated mungbean seedlings. 相似文献
8.
Elicitor, derived from the cell walls of Aspergillus niger, induced rapid generation of reactive oxygen intermediates (ROI), including superoxide anion (O 2−) and hydrogen peroxide (H 2O 2), sequentially followed by phenylalanine ammonia-lyase (PAL) activation and catharanthine biosynthesis in Catharanthus roseus suspension cells. The elicitor-induced PAL activation and catharanthine biosynthesis were blocked by NAD(P)H oxidase inhibitor, diphenylene iodonium (DPI). O 2− generated by the reaction of xanthine/xanthine oxidase (X/XO) triggered PAL activation and catharanthine biosynthesis of C. roseus cells in the absence of elicitor and reversed the inhibitory effect of DPI on elicitor-induced PAL activation and catharanthine biosynthesis. External application of H 2O 2 and catalase had no effect on PAL activity and catharanthine contents of C. roseus cells. The results demonstrated a causal relationship between elicitor-induced oxidative burst and PAL activation in C. roseus suspension cells and suggested a sequence of signaling events from ROI production to PAL activation and catharanthine synthesis. Within this sequence, O 2− rather than H 2O 2 appeared to trigger the subsequent reactions. 相似文献
9.
AbstractApoptosis is an important cell death system that deletes damaged and mutated cells, preventing the induction of cancer. We previously have reported that UV irradiation inhibited the apoptosis induced by serum starvation and cell detachment. This phenomenon is suitable for clarifying the relationship between cancer and the dysregulation of apoptosis by UV irradiation. Here, we have studied the factors responsible for this inhibition of apoptosis, focusing on reactive oxygen species (ROS) and DNA damage. Treatment with xanthine oxidase in the presence of hypoxanthine, which is known to produce superoxide anion (O 2??) and hydrogen peroxide (H 2O 2), inhibited the induction of apoptosis. The xanthine oxidase-induced anti-apoptotic effect was suppressed in the presence of an H 2O 2-eliminating enzyme, catalase, but not in the presence of an O 2??-eliminating enzyme, superoxide dismutase. Treatment with H 2O 2 itself significantly inhibited the induction of apoptosis. Furthermore, the effect of the inhibition of cell death by UVB irradiation and by H 2O 2 treatment decreased in H 2O 2-resistant cells. Although both UVB and H 2O 2 are known to induce DNA damage, other DNA damaging agents, like γ-irradiation and treatment with cisplatin and bleomycin, showed no inhibition of apoptosis. These findings suggested that H 2O 2 was essential to the inhibition of apoptosis, in which DNA damage had no role. 相似文献
10.
Exogenous hydrogen peroxide (H 2O 2) induces oxidative stress and apoptosis in cancer cells. This study evaluated the antiapoptotic effects of pan-caspase and caspase-3, -8, or -9 inhibitors on H 2O 2-treated Calu-6 and A549 lung cancer cells in relation to reactive oxygen species (ROS) and glutathione (GSH). Treatment with 50–500 μM H 2O 2 inhibited the growth of Calu-6 and A549 cells at 24 h and induced apoptosis in these cells. All the tested caspase inhibitors significantly prevented cell death in H 2O 2-treated lung cancer cells. H 2O 2 increased intracellular ROS levels, including that of O 2 ·? , at 1 and 24 h. It also increased the activity of catalase but decreased the activity of SOD. In addition, H 2O 2 triggered GSH deletion in Calu-6 and A549 cells at 24 h. It reduced GSH levels in Calu-6 cells at 1 h but increased them at 24 h. Caspase inhibitors decreased O 2 ·? levels in H 2O 2-treated Calu-6 cells at 1 h and these inhibitors decreased ROS levels, including that of O 2 ·? , in H 2O 2-treated A549 cells at 24 h. Caspase inhibitors partially attenuated GSH depletion in H 2O 2-treated A549 cells and increased GSH levels in these cells at 24 h. However, the inhibitors did not affect GSH deletion and levels in Calu-6 cells at 24 h. In conclusion, H 2O 2 induced caspase-dependent apoptosis in Calu-6 and A549 cells, which was accompanied by increases in ROS and GSH depletion. The antiapoptotic effects of caspase inhibitors were somewhat related to the suppression of H 2O 2-induced oxidative stress and GSH depletion. 相似文献
11.
Peroxidase associated with isolated horseradish cell walls catalyzes the formation of H 2O 2 in the presence of NADH. The reaction is stimulated by various monophenols, especially of coniferyl alcohol. NADH can be provided by a bound malate dehydrogenase. This system is capable of polymerizing coniferyl alcohol yielding an insoluble dehydrogenation polymer. NADH was found to be oxidized by two different mechanisms, one involving Mn 2+, monophenol, and the superoxide radical O 2
·- in a reaction that is not affected by superoxide dismutase, and another one depending on the presence of free O 2
·- and probably of an enzyme-NADH complex. A scheme of these reaction chains, which are thought to be involved in the lignification process, is presented.Abbreviations DHP
dehydrogenation polymer
- GOT
glutamate oxaloacetate transaminase (EC 2.6.1.1)
- LDH
lactate dehydrogenase (pig heart, EC 1.1.1.27)
- MDH
malate dehydrogenase (EC 1.1.1.37)
- pCA
p-coumaric acid
- SOD
superoxide dismutase (EC 1.15.1.1)
- TLC
thin-layer chromatography
- XOD
xanthine oxidase (EC 1.2.3.2) 相似文献
12.
ABSTRACTThis study aimed to investigate the unique antioxidative effects of Japanese moringa products, herbal leaf tea and stem tea, using established free radical assays, focusing on superoxide anion (O 2?) radical generation systems. Hot-water extracts from moringa teas resulted in different but lower scavenging activities than Trolox in four synthetic free radical models. Interestingly, these extracts further showed higher O 2? radical scavenging effects than Trolox in the phenazine methosulfate-NADH-nitroblue tetrazolium and xanthine oxidase assay systems. Incubating human neutrophils in the presence of these tea extracts rather than Trolox effectively suppressed cellular O 2? radical generation. Among the eight known phenolic constituents of moringa leaves, caffeic acid and chlorogenic acid may be responsible for the O 2–specific radical scavenging capacity stronger than that of Trolox. These results suggest that moringa herbal teas are a good source of natural antioxidants for preventing O 2? radical-mediated disorders. Abbreviations: O 2?: superoxide anion; ROS: reactive oxygen species; H 2O 2: hydrogen peroxide; XOD: xanthine oxidase; DPPH: 1,1-diphenyl-2-picrylhydrazyl; ABTS +: 2,2′-azinobis(2-ethylbenzothiazoline-6-sulfonic acid) cation; CPZ +: chlorpromazine cation; PMS: phenazine methosulfate; NBT: nitroblue tetrazolium; PMA: phorbol 12-myristate 13-acetate 相似文献
13.
Information regarding cellular anti-senescence attributes of probiotic bacteria vis-à-vis modulation of senescence-associated secretory phenotype (SASP) and mTOR signaling is very limited. The present study assessed anti-senescence potential of secretory metabolites of probiotic Lactobacillus fermentum (Lact. fermentum) using H2O2-induced model of senescence in 3T3-L1 preadipocytes. Application of H2O2-induced cellular senescence characterized by increased cell size and SA-β-gal activity, activation of SASP and reactive oxygen species (ROS), DNA damage response and induction of cell cycle inhibitors (p53/p21WAF1/p16INK4a). Further, a robust stimulation of the PI3K/Akt/mTOR pathway and AMPK signaling was also observed in H2O2-treated cells. However, exposure of cells to cell-free supernatant of Lact. fermentum significantly attenuated phosphorylation of PI3K/Akt/mTOR pathway and alleviated senescence markers p53, p21WAF1, SA-β-gal, p38MAPK, iNOS, cox-2, ROS, NF-κB, and DNA damage response. These results provide evidence that secretory metabolites of Lact. fermentum can mitigate the development as well as severity of stress-induced senescence thereby indicating its utility for use as anti-aging or age-delaying agent. 相似文献
14.
Col E1 DNA suffers strand scission when exposed to xanthine oxidase acting aerobically on xanthine. Strand scission was prevented by low levels of superoxide dismutase or of catalase. Mannitol, benzoate, or histidine, which scavenge OH · but which react with neither O 2? nor H 2O 2, also prevented strand scission. Replacement of 0.1 mm ethylenediaminetetraacetate by 0.1 mm diethylenetriaminepentaacetate prevented strand scission. Three mechanisms for the production of OH ·, or of a comparably powerful oxidant, by metal-catalyzed interaction of O 2? with H 2O 2, are proposed. 相似文献
15.
Xanthophyllomyces dendrorhous (formerly Phaffia rhodozyma) in shake-flask cultures was exposed to 10–20 mmol/L H 2O 2 at various culture stages, and the astaxanthin production was significantly increased by H 2O 2 fed at 0 or 24 h (exponential phase), but only slightly at 48 h (near stationary phase). The astaxanthin production was enhanced most significantly with double feeding of 10 mmol/L H 2O 2 at 0 and 24 h, reaching a cellular content of 1.30 mg/g cell and a volumetric yield of 10.4 mg/L, which were 83 and 65% higher, respectively, than those of the control (0.71 mg/g cell and 6.3 mg/L). The intracellular catalase (CAT) activity was also increased after H 2O 2 treatment. The increases in CAT and astaxanthin of cells could be detected within 4 h of H 2O 2 treatment. The increase in the astaxanthin content of cells was concomitant with a notable decrease in the β-carotene content. The older yeast cells at late culture stage (120 h), due perhaps in part to their higher astaxanthin contents, were more tolerant to H 2O 2 toxicity than the younger cells (24 h). No enhancement of the astaxanthin biosynthesis was attained when H 2O 2 was added to the yeast culture together with a sufficient amount of exogenous CAT. The results suggest that astaxanthin biosynthesis in X. dendrorhous can be stimulated by H 2O 2 as an antioxidative response. 相似文献
16.
Abstract: Hydrogen peroxide (H 2O 2) is a potent stimulator of signal-responsive phospholipase A 2 (PLA 2) in vascular smooth muscle and cultured endothelial cells. We investigated whether H 2O 2 plays a similar regulatory role in neurons. H 2O 2 did not stimulate a release of arachidonic acid from cultured neurons when applied alone but strongly enhanced the liberation of arachidonic acid evoked by maximally effective concentrations of either glutamate, the glutamate receptor agonist N-methyl-d -aspartate (NMDA), the muscarinic receptor agonist carbachol, the Na +-channel opener veratridine, or the Ca 2+-ionophore ionomycin. The potentiating effects of H 2O 2 were strongly inhibited in the presence of the PLA 2 inhibitor mepacrine, suggesting that the site of action was within the signal responsive arachidonic acid cascade. The enhancing effect of H 2O 2 was not reversed by protein kinase C inhibitors (chelerythrine chloride or GF 109203X) nor was it mimicked by phorbol ester treatment. H 2O 2 alone strongly enhanced the levels of immunodetectable activated mitogen-activated protein kinase (activated MAP kinases ERK1 and ERK2) in a Ca 2+-dependent manner and this effect was additive with increases in the levels of activated MAP kinase evoked by glutamate. The enhanced release of arachidonic acid, however, was not clearly reversed by the MAP kinase kinase (MEK) inhibitor PD 98059, although this treatment effectively abolished H 2O 2 activation of MAP kinase. Thus, MAP kinase activation and Ca 2+-dependent arachidonic acid release are regulated by oxidative stress in cultured striatal neurons. 相似文献
17.
The mechanisms of sensing and signalling of heat and oxidative stresses are not well understood. The central question of this
paper is whether in plant cells oxidative stress, in particular H 2O 2, is required for heat stress- and heat shock factor (HSF)-dependent expression of genes. Heat stress increases intracellular
accumulation of H 2O 2 in Arabidopsis cell culture. The accumulation was greatly diminished using ascorbate as a scavenger or respectively diphenyleneiodonium
chloride (DPI) as an inhibitor of reactive oxygen species production. The mRNA of heat shock protein (HSP) genes, exemplified
by Hsp17.6, Hsp18.2, and the two cytosolic ascorbate peroxidase genes Apx1, Apx2, reached similar levels by moderate heat stress (37°C) or by treatment with H 2O 2, butylperoxide and diamide at room temperature. The heat-induced expression levels were significantly reduced in the presence
of ascorbate or DPI indicating that H 2O 2 is an essential component in the heat stress signalling pathway. Rapid (15 min) formation of heat shock promoter element
(HSE) protein-binding complex of high molecular weight in extracts of heat-stressed or H 2O 2-treated cells and the inability to form this complex after ascorbate treatment suggests that oxidative stress affects gene
expression via HSF activation and conversely, that H 2O 2 is involved in HSF activation during the early phase of heat stress. The heat stress induction of a high mobility HSE-binding
complex, characteristic for later phase of heat shock response, was blocked by ascorbate and DPI. H 2O 2 was unable to induce this complex suggesting that H 2O 2 is involved only in the early stages of HSF activation. Significant induction of the genes tested after diamid treatment
and moderate expression of the sHSP genes in the presence of 50 mM ascorbate at 37°C occurred without activation of HSF, indicating
that other mechanisms may be involved in stress signalling.
Electronic Supplementary Material Supplementary material is available for this article at http//dx.doi.org/10.1007/s11103-006-0045-4
Roman A. Volkov and Irina I. Panchuk contributed equally 相似文献
18.
The hypoxanthine — xanthine oxidase system generates an extracellular flux of superoxide anion radical (O 2?) and hydrogen peroxide (H 2O 2). Catalase but not superoxide dismutase (SOD) protects V79 cells exposed to the hypoxanthine — xanthine oxidase system, showing that H 2O 2 is the major reactive oxygen species involved in the cytotoxicity of such a system. In contrast to SOD, the lipophilic SOD like compound CuII (diisopropylsalicylate) 2 (CuDIPS) exhibits some protection at non cytotoxic concentration. It is also found that methanol partially protects cells exposed to the hypoxanthine-xanthine oxidase system. It appears that in our experimental conditions (temperature, ionic strength and pH) the protective effect afforded by methanol and CuDIPS is due to the inhibition of the xanthine oxidase activity. 相似文献
19.
Abstract: Previous research has suggested that the initial effects of cellular free radical neurotoxic insult involve large increases in intracellular Ca 2+. However, the exact role of oxidative stress on the various parameters involved in these increases has not been specified. The present experiments were performed to examine these parameters in PC12 cells exposed to 5, 25, or 300 µ M H 2O 2 for 30 min in growth medium alone or containing either nifedipine (L-type Ca 2+ antagonist), conotoxin (N-type antagonist), Trolox (vitamin E analogue), or α-phenyl- n- tert-butylnitrone (nitrone trapping agent; PBN). The concentrations of H 2O 2 were chosen by examining the degree of cell killing induced by exposure to graded concentrations of H 2O 2. The 5 and 25 µ M concentrations of H 2O 2 produced no significant cell killing at either 30 min or 24 h after treatment, whereas the 300 µ M concentration produced a moderate degree of cell killing that did not increase between the two times. Fluorescent imaging was used to visualize intracellular Ca 2+ changes in fura-2-loaded cells. Baseline (pre-30 m M KCI) Ca 2+ levels were increased significantly by H 2O 2 treatment (e.g., 300 µ M, 200%), but the rise in the level of free intracellular Ca 2+ after KCI stimulation (i.e., peak) was decreased (e.g., 300 µ M, 50%) and the cell's ability to sequester or extrude the excess Ca 2+ (i.e., Ca 2+ recovery time) after depolarization was decreased significantly. All compounds prevented baseline Ca 2+ increases and, with the exception of conotoxin, antagonized the peak decreases in Ca 2+. It is interesting that after 300 µ M H 2O 2 exposure, only Trolox was partially effective in preventing these deficits in recovery. Conotoxin increased the decrement recovery in the absence of H 2O 2. However, in cells exposed to 5 or 25 µ M H 2O 2, conotoxin as well as the other agents were effective in preventing the deficits in recovery. 相似文献
20.
Antioxidative responses and proline accumulation induced by exogenous H 2O 2 were investigated in the callus from halophyte Nitraria tangutorum Bobr. H 2O 2-treated callus exhibited higher H 2O 2 content than untreated callus. The activities of catalase (CAT) and peroxidase (POD) significantly increased in the callus
treated with H 2O 2, while ascorbate peroxidase (APX) activity decreased. In addition, significantly enhanced proline content was observed in
the callus treated by H 2O 2, which could be alleviated by H 2O 2 scavenger dimethylthiourea and calcium (Ca) chelator ethylene glycol bis-(β-aminoethyl ether)-N,N,N′,N′-tetra-acetic acid
(EGTA). Moreover, γ-glutamyl kinase (GK) activity increased in H 2O 2-treated callus, but proline dehydrogenase (PDH) activity decreased significantly, and the reduction was partly abolished
by EGTA or Ca channel blocker verapamil. Assays using a scanning electron microscope showed significantly enhanced Ca content
in H 2O 2-treated callus. 相似文献
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