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1.
Although arsenic is an infamous carcinogen, it has been effectively used to treat acute promyelocytic leukemia, and can induce
cell cycle arrest or apoptosis in human solid tumors. Previously, we had demonstrated that opposing effects of ERK1/2 and
JNK on p21 expression in response to arsenic trioxide (As2O3) are mediated through the Sp1 responsive elements of the p21 promoter in A431 cells. Presently, we demonstrate that Sp1,
and c-Jun functionally cooperate to activate p21 promoter expression through Sp1 binding sites (−84/−64) by using DNA affinity
binding, chromatin immunoprecipitation, and promoter assays. Surprisingly, As2O3-induced c-Jun(Ser63/73) phosphorylation can recruit TGIF/HDAC1 to the Sp1 binding sites and then suppress p21 promoter activation.
We suggest that, after As2O3 treatment, the N-terminal domain of c-Jun phosphorylation by JNK recruits TGIF/HDAC1 to the Sp1 sites and then represses p21
expression. That is, TGIF is involved in As2O3-inhibited p21 expression, and then blocks the cell cycle arrest. 相似文献
2.
Ros Barceló A 《Planta》2005,220(5):747-756
Lignification in Zinnia elegans L. stems is characterized by a burst in the production of H2O2, the apparent fate of which is to be used by xylem peroxidases for the polymerization of p-hydroxycinnamyl alcohols into lignins. A search for the sites of H2O2 production in the differentiating xylem of Z. elegans stems by the simultaneous use of optical (bright field, polarized light and epi-polarization) and electron-microscope tools revealed that H2O2 is produced on the outer-face of the plasma membrane of both differentiating (living) thin-walled xylem cells and particular (non-lignifying) xylem parenchyma cells. From the production sites it diffuses to the differentiating (secondary cell wall-forming) and differentiated lignifying xylem vessels. H2O2 diffusion occurs mainly through the continuous cell wall space. Both the experimental data and the theoretical calculations suggest that H2O2 diffusion from the sites of production might not limit the rate of xylem cell wall lignification. It can be concluded that H2O2 is produced at the plasma membrane in differentiating (living) thin-walled xylem cells and xylem parenchyma cells associated to xylem vessels, and that it diffuses to adjacent secondary lignifying xylem vessels. The results strongly indicate that non-lignifying xylem parenchyma cells are the source of the H2O2 necessary for the polymerization of cinnamyl alcohols in the secondary cell wall of lignifying xylem vessels. 相似文献
3.
Jingjing Jia Ting Zhang Jieshan Chi Xiaoma Liu Jingjing Sun Qizhi Xie Sijia Peng Changyan Li Li Yi 《Neurochemical research》2018,43(7):1439-1453
4.
S. R. Sampson E. Bucris M. Horovitz-Fried A. Parnas S. Kahana G. Abitbol M. Chetboun T. Rosenzweig C. Brodie S. Frankel 《Apoptosis : an international journal on programmed cell death》2010,15(10):1165-1176
Insulin resistance results, in part, from impaired insulin signaling in insulin target tissues. Consequently, increased levels
of insulin are necessary to control plasma glucose levels. The effects of elevated insulin levels on pancreatic beta (β) cell
function, however, are unclear. In this study, we investigated the possibility that insulin may influence survival of pancreatic
β cells. Studies were conducted on RINm, RINm5F and Min-6 pancreatic β-cells. Cell death was induced by treatment with H2O2, and was estimated by measurements of LDH levels, viability assay (Cell-Titer Blue), propidium iodide staining and FACS analysis,
and mitochondrial membrane potential (JC-1). In addition, levels of cleaved caspase-3 and caspase activity were determined.
Treatment with H2O2 increased cell death; this effect was increased by simultaneous treatment of cells with insulin. Insulin treatment alone
caused a slight increase in cell death. Inhibition of caspase-3 reduced the effect of insulin to increase H2O2-induced cell death. Insulin increased ROS production by pancreatic β cells and increased the effect of H2O2. These effects were increased by inhibition of IR signaling, indicative of an effect independent of the IR cascade. We conclude
that elevated levels of insulin may act to exacerbate cell death induced by H2O2 and, perhaps, other inducers of apoptosis. 相似文献
5.
It was shown that tobacco leaf treatment with 100 mM H2O2 increased their content of endogenous H2O2 and activities of catalase and hydrolases (acid phosphatase, proteases, and RNase) and also caused various changes in the cell structure. In this case, programmed cell death (PCD) occurred in some cells, which was observed as chromatin condensation, cytoplasm collapse, etc. In the meantime, many cells displayed organelle activation rather than PCD. It is suggested that cells that undergo H2O2-dependent PCD release signaling molecules inducing protective mechanisms against oxidative stress in neighboring cells not exhibiting PCD. 相似文献
6.
Marcos Roberto de Oliveira Gustavo da Costa Ferreira Alessandra Peres Simone Morelo Dal Bosco 《Molecular neurobiology》2018,55(2):968-979
The phenolic diterpene carnosic acid (CA, C20H28O4) exerts antioxidant, anti-inflammatory, anti-apoptotic, and anti-cancer effects in mammalian cells. CA activates the nuclear factor erythroid 2-related factor 2 (Nrf2), among other signaling pathways, and restores cell viability in several in vitro and in vivo experimental models. We have previously reported that CA affords mitochondrial protection against various chemical challenges. However, it was not clear yet whether CA would prevent chemically induced impairment of the tricarboxylic acid cycle (TCA) function in mammalian cells. In the present work, we found that a pretreatment of human neuroblastoma SH-SY5Y cells with CA at 1 μM for 12 h prevented the hydrogen peroxide (H2O2)-induced impairment of the TCA enzymes (aconitase, α-ketoglutarate dehydrogenase (α-KGDH), succinate dehydrogenase (SDH)) and abolished the inhibition of the complexes I and V and restored the levels of ATP by a mechanism associated with Nrf2. CA also exhibited antioxidant abilities by enhancing the levels of reduced glutathione (GSH) and decreasing the content oxidative stress markers (cellular 8-oxo-2′-deoxyguanosine (8-oxo-dG), and mitochondrial malondialdehyde (MDA), protein carbonyl, and 3-nitrotyrosine). Silencing of Nrf2 by small interfering RNA (siRNA) abrogated the protective effects elicited by CA in mitochondria of SH-SY5Y cells. Therefore, CA prevented the H2O2-triggered mitochondrial impairment by an Nrf2-dependent mechanism. The specific role of Nrf2 in ameliorating the function of TCA enzymes function needs further research. 相似文献
7.
Vanadium is an environmentally toxic metal with peculiar and sometimes contradictory cellular effects. It is insulin-mimetic,
it can either stimulate cell growth or induce cell death, and it has both mutagenic and antineoplastic properties. However,
the mechanisms involved in those effects are poorly understood. Several studies suggest that H2O2 is involved in vanadate-induced cell death, but it is not known whether cellular sensitivity to vanadate is indeed related
to H2O2 generation. In the present study, the sensitivity of four cell lines from different origins (K562, K562-Lucena 1, MDCK, and
Ma104) to vanadate and H2O2 was evaluated and the production of H2O2 by vanadate was analyzed by flow cytometry. We show that cell lines very resistant to H2O2 (K562, K562-Lucena 1, and Ma104 cells) are much more sensitive to vanadate than MDCK, a cell line relatively susceptible
to H2O2, suggesting that vanadate-induced cytotoxicity is not directly related to H2O2 responsiveness. In accordance, vanadate concentrations that reduced cellular viability to approximately 60–70% of the control
(10 μmol/L) did not induce H2O2 formation. A second hypothesis, that peroxovanadium (PV) compounds, produced once vanadate enters into the cells, are responsible
for the cytotoxicity, was only partially confirmed because MDCK cells were resistant to both vanadate and PV compounds (10 μmol/L
each). Therefore, our results suggest that vanadate toxicity occurs by two distinct pathways, one dependent on and one independent
of H2O2 production. 相似文献
8.
9.
Xiao-hui Chen Xue Zhou Xiao-yu Yang Zhi-bin Zhou Di-han Lu Ying Tang Ze-min Ling Li-hua Zhou Xia Feng 《Cellular and molecular neurobiology》2016,36(4):541-551
Propofol (2,6-diisopropylphenol) is a widely used general anesthetic with anti-oxidant activities. This study aims to investigate protective capacity of propofol against hydrogen peroxide (H2O2)-induced oxidative injury in neural cells and whether the anti-oxidative effects of propofol occur through a mechanism involving the modulation of NADPH oxidase (NOX) in a manner of calcium-dependent. The rat differentiated PC12 cell was subjected to H2O2 exposure for 24 h to mimic a neuronal in vitro model of oxidative injury. Our data demonstrated that pretreatment of PC12 cells with propofol significantly reversed the H2O2-induced decrease in cell viability, prevented H2O2-induced morphological changes, and reduced the ratio of apoptotic cells. We further found that propofol attenuated the accumulation of malondialdehyde (biomarker of oxidative stress), counteracted the overexpression of NOX core subunit gp91phox (NOX2) as well as the NOX activity following H2O2 exposure in PC12 cells. In addition, blocking of L-type Ca2+ channels with nimodipine reduced H2O2-induced overexpression of NOX2 and caspase-3 activation in PC12 cells. Moreover, NOX inhibitor apocynin alone or plus propofol neither induces a significant downregulation of NOX activity nor increases cell viability compared with propofol alone in the PC12 cells exposed to H2O2. These results demonstrate that the protective effects of propofol against oxidative injury in PC12 cells are mediated, at least in part, through inhibition of Ca2+-dependent NADPH oxidase. 相似文献
10.
Izawa S Kono K Mimura K Kawaguchi Y Watanabe M Maruyama T Fujii H 《Cancer immunology, immunotherapy : CII》2011,60(12):1801-1810
Human NK cells can be divided into two subsets, CD56dimCD16(+)NK and CD56brightCD16(−)NK cells, based on their expression of CD56 and CD16. In the present study, we analyzed the relationship between CD56dim/CD56bright NK cells and H2O2 in tumor-infiltrating NK cells in patients with gastric (n = 50) and esophageal (n = 35) cancer. The ratio of CD56dim NK cells infiltrating tumors gradually decreased according to disease progression. H2O2 was abundantly produced within tumor microenvironments, and there was an inverse correlation between CD56dim NK cell infiltration and H2O2 production. CD56dim NK cells are more sensitive to apoptosis induced by physiological levels of H2O2 than CD56bright NK cells. Furthermore, the exposure of NK cells to H2O2 resulted in the impairment of ADCC activity. In conclusion, H2O2 produced within tumor microenvironments inversely correlated with the infiltration of CD56dim NK cells, possibly due to their preferentially induced cell death. These observations may explain one of the mechanisms behind
NK cell dysfunction frequently observed in tumor microenvironments. 相似文献
11.
This study employed confocal laser scanning microscopy to monitor the effect of H2O2 on cytosolic as well as mitochondrial calcium (Ca2+) concentrations, mitochondrial inner membrane potential (m) and flavine adenine dinucleotide (FAD) oxidation state in isolated mouse pancreatic acinar cells. The results show that incubation of pancreatic acinar cells with H2O2, in the absence of extracellular Ca2+ ([Ca2+]o) led to an increase either in cytosolic and in mitochondrial Ca2+ concentration. Additionally, H2O2 induced a depolarization of mitochondria and increased oxidized FAD level. Pretreatment of cells with the mitochondrial inhibitors rotenone or cyanide inhibited the response induced by H2O2 on mitochondrial inner membrane potential but failed to block oxidation of FAD in the presence of H2O2. However, the H2O2-evoked effect on FAD state was blocked by pretreatment of cells with the mitochondrial uncoupler, carbonyl cyanide p-trifluoromethoxy-phenylhydrazone (FCCP). On the other hand, perfusion of cells with thapsigargin (Tps), an inhibitor of the SERCA pump, led to an increase in mitochondrial Ca2+ concentration and in oxidized FAD level, and depolarized mitochondria. Pretreatment of cells with thapsigargin inhibited H2O2-evoked changes in mitochondrial Ca2+ concentration but not those in membrane potential and FAD state. The present results have indicated that H2O2 can evoke marked changes in mitochondrial activity that might be due to the oxidant nature of H2O2. This in turn could represent the mechanism of action of ROS to induce cellular damage leading to cell dysfunction and generation of pathologies in the pancreas. (Mol Cell Biochem 269: 165–173, 2005) 相似文献
12.
In this study, the effect of aucubin on H2O2-induced apoptosis was studied by using a rat pheochromocytoma (PC12) cell line. We have analyzed the apoptosis of H2O2-induced PC12 cells, H2O2-induced apoptosis appeared to correlate with lower Bcl-2 expression, higher Bax expression and sequential activation of caspase-3
leading to cleavage of poly-ADP-ribose polymerase (PARP). Aucubin not only inhibited lower Bcl-2 expression, high Bax expression,
but also modulated caspase-3 activation, PARP cleavage, and eventually protected against H2O2-induced apoptosis. These results indicated that aucubin can obstruct H2O2-induced apoptosis by regulating of the expression of Bcl-2 and Bax, as well as suppression of caspases cascade activation. 相似文献
13.
Asrin Rahimi Iraj Amiri Amaneh Mohammadi Roushandeh Zoleikha Golipour Choshali Zohreh Alizadeh Tayebeh Artimani Saeid Afshar Sara Soleimani Asl 《Biotechnology letters》2018,40(3):609-615
Objective
To investigate the effect of H2O2 on the migration and antioxidant defense of mesenchymal stem cells (MSCs) and the neurotrophic effects of H2O2-treated MSCs on spinal cord injury (SCI).Results
Sublethal concentrations of H2O2 decreased cell migration and expression of CXCR4 and CCR2 as well as Nrf2 expression in MSCs. In the second phase, transplantation of treated and untreated MSCs to SCI caused minor changes in locomotor dysfunction. There was a significantly difference between cell-treated and spinal cord injury groups in expression of BDNF (brain-derived neurotrophic factor). Transplantation of H2O2-treated cells caused an increase in BDNF expression compared to non-treated cells.Conclusion
Transplantation of H2O2-treated stem cells may have protective effects against SCI through by increasing neurotrophic factors.14.
In2O3 nanoparticle-assembled nanorods with distinct surface morphologies have been newly synthesized by a dehydration process of
self-assembled In(OH)3 nanorods obtained from a liquid-based route. The reaction mechanism and the structural transformation between these two one-dimensional
nanorods, In2O3 and In(OH)3, were precisely characterized by means of various qualitative and quantitative analyses with X-ray scattering simulations.
The broad absorption band in the UV–visible spectrum evidently originates from the nanoparticle-assembling effect within the
In2O3 nanorods. An intensive photoluminescence emission at 440 nm observed under an excitation wavelength of 325 nm is attributed
to the existence of oxygen vacancies within the In2O3 nanorods. 相似文献
15.
Jacqueline A. Jordan Ashley M. Verhoff Julie E. Morgan David G. Fischer 《In vitro cellular & developmental biology. Animal》2009,45(10):602-613
Prior chemical and physical analysis of lunar soil suggests a composition of dust particles that may contribute to the development
of acute and chronic respiratory disorders. In this study, fine Al2O3 (0.7 μm) and fine SiO2 (mean 1.6 μm) were used to assess the cellular uptake and cellular toxicity of lunar dust particle analogs. Respiratory cells,
murine alveolar macrophages (RAW 264.7) and human type II epithelial (A549), were cultured as the in vitro model system. The
phagocytic activity of both cell types using ultrafine (0.1 μm) and fine (0.5 μm) fluorescent polystyrene beads was determined.
Following a 6-h exposure, RAW 264.7 cells had extended pseudopods with beads localized in the cytoplasmic region of cells.
After 24 h, the macrophage cells were rounded and clumped and lacked pseudopods, which suggest impairment of phagocytosis.
A549 cells did not contain beads, and after 24 h, the majority of the beads appeared to primarily coat the surface of the
cells. Next, we investigated the cellular response to fine SiO2 and Al2O3 (up to 5 mg/ml). RAW 264.7 cells exposed to 1.0 mg/ml of fine SiO2 for 6 h demonstrated pseudopods, cellular damage, apoptosis, and necrosis. A549 cells showed slight toxicity when exposed
to fine SiO2 for the same time and dose. A549 cells had particles clustered on the surface of the cells. Only a higher dose (5.0 mg/ml)
of fine SiO2 resulted in a significant cytotoxicity to A549 cells. Most importantly, both cell types showed minimal cytotoxicity following
exposure to fine Al2O3. Overall, this study suggests differential cellular toxicity associated with exposure to fine mineral dust particles. 相似文献
16.
The histochemical and cytochemical localization of abscisic acid (ABA)-induced H2O2 production in leaves of maize (Zea mays L.) plants were examined, using 3,3-diaminobenzidine (DAB) and CeCl3 staining, respectively, and the relationship between ABA-induced H2O2 production and ABA-induced subcellular activities of antioxidant enzymes was studied. H2O2 generated in response to ABA treatment was detected within 0.5 h in major veins of the leaves and maximized at about 2–4 h. In mesophyll and bundle sheath cells, ABA-induced H2O2 accumulation was observed only in apoplast, and the greatest accumulation occurred in the walls of mesophyll cells facing large intercellular spaces. Meanwhile, ABA treatment led to a significant increase in the activities of the leaf chloroplastic and cytosolic antioxidant enzymes superoxide dismutase (SOD), ascorbate peroxidase (APX) and glutathione reductase (GR), and pretreatment with the NADPH oxidase inhibitor diphenyleneiodonium (DPI), the O
2
−
scavenger Tiron and the H2O2 scavenger dimethylthiourea (DMTU) almost completely arrested the increase in the activities of these antioxidant enzymes. Our results indicate that the accumulation of apoplastic H2O2 is involved in the induction of the chloroplastic and cytosolic antioxidant enzymes. Moreover, an oxidative stress induced by paraquat (PQ), which generates O
2
−
and then H2O2 in chloroplasts, also up-regulated the activities of the chloroplastic and cytosolic antioxidant enzymes, and the up-regulation was blocked by the pretreatment with Tiron and DMTU. These data suggest that H2O2 produced at a specific cellular site could coordinate the activities of antioxidant enzymes in different subcellular compartments. 相似文献
17.
Kun Yan Wei Chen Guoyou Zhang Sheng Xu Zhouli Liu Xingyuan He Lanlan Wang 《Acta Physiologiae Plantarum》2010,32(2):375-385
Using open top chambers, the effects of elevated O3 (80 nmol mol−1) and elevated CO2 (700 μmol mol−1), alone and in combination, were studied on young trees of Quercus mongolica. The results showed that elevated O3 increased malondialdehyde content and decreased photosynthetic rate after 45 days of exposure, and prolonged exposure (105 days)
induced significant increase in electrolyte leakage and reduction of chlorophyll content. All these changes were alleviated
by elevated CO2, indicating that oxidative stress on cell membrane and photosynthesis was ameliorated. After 45 days of exposure, elevated
O3 stimulated activities of superoxide dismutase (SOD, EC 1.15.1.1) and ascorbate peroxidase (APX, EC 1.11.1.11), but the stimulation
was dampened under elevated CO2 exposure. Furthermore, ascorbate (AsA) and total phenolics contents were not higher in the combined gas treatment than those
in elevated O3 treatment. It indicates that the protective effect of elevated CO2 against O3 stress was achieved hardly by enhancing ROS scavenging ability after 45 days of exposure. After 105 days of exposure, elevated
O3 significantly decreased activities of SOD, catalase (CAT, EC 1.11.1.6) and APX and AsA content. Elevated CO2 suppressed the O3-induced decrease, which could ameliorate the oxidative stress in some extent. In addition, elevated CO2 increased total phenolics content in the leaves both under ambient O3 and elevated O3 exposure, which might contribute to the protection against O3-induced oxidative stress as well. 相似文献
18.
The development of nanotechnologies has increased the amount of manufactured metal oxide nanoparticles in the environment. In the view of nanoparticle dispersion to the environment, assessment of their toxicity becomes very crucial. Aluminum oxide (Al2O3) nanoparticles have wide range of use in industry as well as personal care products. The aim of this study was to evaluate the dose dependent effects of 13-nm-sized Al2O3 nanoparticles on wheat correlating with the appearance of enzymatic and non-enzymatic antioxidant defense response. Wheat roots were exposed to different concentrations of Al2O3 nanoparticles (5, 25 and 50 mg mL?1) for 96 h. The effects of Al2O3 nanoparticles were studied using different parameters such as H2O2 content, superoxide dismutase and catalase activity, lipid peroxidation, total proline, photosynthetic pigment and anthocyanin content. The results indicated that while Al2O3 nanoparticles caused a dose dependent increase in H2O2 content, superoxide dismutase activity, lipid peroxidation and proline contents, the catalase activity was decreased in compare the control. Moreover, total chlorophyll, chlorophyll a, carotenoids and anthocyanin contents reduced in the highest concentration 50 mg mL?1. In conclusion, Al2O3 nanoparticles caused oxidative stress in wheat after 96 h. 相似文献
19.
Gan FF Nagle AA Ang X Ho OH Tan SH Yang H Chui WK Chew EH 《Apoptosis : an international journal on programmed cell death》2011,16(8):856-867
Shogaols have been previously reported to induce cancer cell death via multiple mechanisms, among which one analog 6-shogaol
has been reported to cause microtubule damage through specific reaction with sulfhydryl groups in tubulin. In this study,
a series of shogaols with different side chain lengths (4-, 6-, 8- and 10-shogaol) was synthesized and evaluated for antiproliferative
activity in HCT 116 colon carcinoma and SH-SY5Y neuroblastoma cells. 4- and 6-shogaol were identified as lead compounds possessing
the strongest antiproliferative activity. In the soft agar assay, the lead shogaols displayed dose-dependent inhibition on
cancer cell colony formation under anchorage-independent conditions. Using HCT 116 as the selected cancer cell line, the molecular
events linking shogaols-induced G2/M cell cycle arrest to apoptosis characterized by caspase 3 and PARP cleavage were investigated. At sublethal concentrations,
the halt at G2/M phase was alleviated along time and cells survived. Conversely, proapoptotic concentrations of 4- and 6-shogaol induced
irreversible G2/M arrest that was at least in part associated with down-regulation of cell cycle checkpoint proteins cdk1, cyclin B and cdc25C,
as well as spindle assembly checkpoint proteins mad2, cdc20 and survivin. A dose- and time-dependent accumulation of insoluble
tubulin in the insoluble fractions of cell lysates provided evidence that G2 checkpoint failure led to disruption of microtubule turnover. In summary, our results conclude that shogaols cause apoptosis
by inducing aberrant mitosis at least through the attenuation of cell cycle and spindle assembly checkpoint proteins. 相似文献
20.
This study examined the effects of season-long exposure of Chinese pine (Pinus tabulaeformis) to elevated carbon dioxide (CO2) and/or ozone (O3) on indole-3-acetic acid (IAA) content, activities of IAA oxidase (IAAO) and peroxidase (POD) in needles. Trees grown in
open-top chambers (OTC) were exposed to control (ambient O3, 55 nmol mol−1 + ambient CO2, 350 μmol mol−1, CK), elevated CO2 (ambient O3 + high CO2, 700 μmol mol−1, EC) and elevated O3 (high O3, 80 ± 8 nmol mol−1 + ambient CO2, EO) OTCs from 1 June to 30 September. Plants grown in elevated CO2 OTC had a growth increase of axial shoot and needle length, compared to control, by 20% and 10% respectively, while the growth
in elevated O3 OTC was 43% and 7% less respectively, than control. An increase in IAA content and POD activity and decrease in IAAO activity
were observed in trees exposed to elevated CO2 concentration compared with control. Elevated O3 decreased IAA content and had no significant effect on IAAO activity, but significantly increased POD activity. When trees
pre-exposed to elevated CO2 were transferred to elevated O3 (EC–EO) or trees pre-exposed to elevated O3 were transferred to elevated CO2 (EO–EC), IAA content was lower while IAAO activity was higher than that transferred to CK (EC–CK or EO–CK), the change in
IAA content was also related to IAAO activity. The results indicated that IAAO and POD activities in Chinese pine needles
may be affected by the changes in the atmospheric environment, resulting in the change of IAA metabolism which in turn may
cause changes in Chinese pine’s growth.
An erratum to this article can be found at 相似文献