共查询到20条相似文献,搜索用时 31 毫秒
1.
In this study, the release of mitochondrial proapoptotic intermembrane space proteins induced by exogenous C2-ceramide in human colon carcinoma (HT-29) cell line was investigated. HT-29 cells were treated with 12.5, 25 and 50 μmol/L C2-ceramide in vitro. Flow cytometer was used to detect the mitochondrial membrane potential (△Ψm). Subcellular fractions were extracted by Mitochondrial/Cytosol Fractionation Kit after C2-ceramide treatment for 24 h. SDS-PAGE was used to determine the level of cytochrome c (Cyt c), high temperature requirement A2 (HtrA2) and second mitochondrial-derived activator of caspases (Smac) released from mitochondria, the expression of X-linked inhibitor of apoptosis protein (XIAP) and caspase-3 for 24 h. The results showed that △Ψm began to decrease from 6 h after 25 and 50 μmol/L C2-ceramide treatment (P<0.05) and cyclosporin A (CsA) could inhibit the collapse of △Ψm through regulating mitochondrial membrane permeability transition pore. There was no effect of C2-ceramide on the expression of Cyt c, HtrA2 and Smac in the total levels. 12.5, 25 and 50 μmol/L C2-ceramide could induce Cyt c, HtrA2 and Smac to release from mitochondria to cytosol and down-regulate the expression of XIAP (P<0.05). Also there was expression of cleaved caspase-3 with C2-ceramide treatment. After the treatment with caspase inhibitor, C2-ceramide still induced the release of Cyt c and HtrA2, but Smac did not. Therefore, C2-ceramide could induce apoptosis of HT-29 cells through the mitochondria pathway. The release of Cyt c, HtrA2 and Smac from mitochondria did not occur via the same mechanism, the release of Cyt c and HtrA2 was caspase-independent and the release of Smac was caspase-dependent. 相似文献
2.
Apoptosis and necrosis are distinct forms of cell death that occur in response to various agents. We studied the action of N-Acetyl-D-sphingosine (C2-ceramide) or N-hexanoyl-D-sphyngosine (C6-ceramide) in human hepatoma HepG2 cell line. The cells were treated in vitro for 1–24 h. Cell toxicity was evaluated by MTT assay. DNA content was estimated by gel electrophoresis and flow cytometry. Measurement of mitochondrial respiration, analysis of cytochrome c release and caspase-3 activation were assessed in order to determine if either of these events in the induction of apoptosis and/or necrosis was predominant. We have demonstrated that C2 and C6-ceramide were cytotoxic in a time and dose-dependent manner. After 24 h of treatment with 100 M of C2 and C6 the morphology (May-Giemsa staining) of treated cells displayed an apoptotic phenotype in C6-treated cells, confirmed by a high (sub-G1 peak > 20%) proportion by flow cytometry while a necrotic morphology was observed after C2-ceramide treatment, confirmed by DNA smearing in DNA electrophoresis. After C6-ceramide incubation, the respiratory chain was functional only slightly inhibited (20%), there was production of ATP, cytochrome c release without ROS production, activation of caspase-3 and induction of apoptosis. On the contrary, C2-ceramide inhibit the respiratory chain more intensely (80%) increased significantly ROS production, which resulted in an arrest of ATP production, no cytochrome c release and absence of caspase-3 activation. Finally after complete exhaustion of intracellular ATP, mitochondrial explosion induce necrotic cell death. In conclusion, evidence suggest that mitochondrial respiratory chain function is essential for controlling the decision of the cell to enter a apoptotic or necrosis process. 相似文献
3.
Buratta M Piccotti L Giannini S Gresele P Roberti R Corazzi L 《The Journal of membrane biology》2006,212(3):199-210
In brain mitochondria, phosphate- and Ca2+-dependent cytocrome c (cyt c) release reveals pools that interact differently with the inner membrane. Detachment of the phosphate-dependent pool did
not influence the pool released by Ca2+. Cyt c pools were also detected in a system of cyt c reconstituted in cardiolipin (CL) liposomes. Gradual binding of cyt c (1 nmol) to CL/2–[12-(7-nitrobenz- 2-oxa-1,3-diazol-4-yl)amino]dodecanoyl-1-hexadecan oyl-sn-glycero-3-phosphocholine (NBDC12-HPC) liposomes (10 nmol) produced NBD fluorescence quenching up to 0.4 nmol of added protein. Additional bound cyt c did not produce quenching, suggesting that cyt c-CL interactions originate distinct cyt c pools. Cyt c was removed from CL/NBDC12-HPC liposomes by either phosphate or Ca2+, but only Ca2+ produced fluorescence dequenching and leakage of encapsulated 8-aminonaphthalene-1,3,6-trisulfonic acid/p-xylene-bis-pyridinium bromide. In mitochondria, complex IV activity and mitochondrial membrane potential (Δψm) were not affected by the release of the phosphate-dependent cyt c pool. Conversely, removal of cyt c by Ca2+ caused inhibition of complex IV activity and impairment of Δψm. In a reconstituted system of mitochondria, nuclei and supernatant, cyt c detached from the inner membrane was released outside mitochondria and triggered events leading to DNA fragmentation. These
events were prevented by enriching mitochondria with exogenous CL or by sequestering released cyt c with anti-cyt c antibody. 相似文献
4.
Resveratrol, a natural polyphenolic antioxidant, has been reported to possess the cancer chemopreventive potential in wide
range by means of triggering tumor cells apoptosis through various pathways. It induced apoptosis through the activation of
the mitochondrial pathway in some kinds of cells. In the present reports, we showed that resveratrol-induced HepG2 cell apoptosis
and mitochondrial dysfunction was dependent on the induction of the mitochondrial permeability transition (MPT), because resveratrol
caused the collapse of the mitochondrial membrane potential (ΔΨm) with the concomitant release of cytochrome c (Cyt.c). In addition, resveratrol induced a rapid and sustained elevation of
intracellular [Ca2+], which compromised the mitochondrial ΔΨm and triggered the process of HepG2 cell apoptosis. In permeabilized HepG2 cells, we further demonstrated that the effect
of the resveratrol was indeed synergistic with that of Ca2+ and Ca2+ is necessary for resveratrol-induced MPT opening. Calcium-induced calcium release from mitochondria (mCICR) played a key
role in mitochondrial dysfunction and cell apoptosis: (1) mCICR inhibitor, ruthenium red (RR), prevent MPT opening and Cyt.c
release; and (2) RR attenuated resveratrol-induced HepG2 cell apoptotic death. Furthermore, resveratrol promotes MPT opening
by lowering Ca2+-threshold. These data suggest modifying mCICR and Ca2+ threshold to modulate MPT opening may be a potential target to control cell apoptosis induced by resveratrol.
Xuemei Tian—Foundation item: Chinese National Natural Science Foundation (No.30300455). 相似文献
5.
Małgorzata Budzińska Hanna Gałgańska Andonis Karachitos Małgorzata Wojtkowska Hanna Kmita 《Journal of bioenergetics and biomembranes》2009,41(4):361-367
Available data indicate that superoxide anion (O2•− ) is released from mitochondria, but apart from VDAC (voltage dependent anion channel), the proteins involved in its transport
across the mitochondrial outer membrane still remain elusive. Using mitochondria of the yeast Saccharomyces cerevisiae mutant depleted of VDAC (Δpor1 mutant) and the isogenic wild type, we studied the role of the TOM complex (translocase of the outer membrane) in the efflux
of O2•− from the mitochondria. We found that blocking the TOM complex with the fusion protein pb2-DHFR decreased O2•− release, particularly in the case of Δpor1 mitochondria. We also observed that the effect of the TOM complex blockage on O2•− release from mitochondria coincided with the levels of O2•− release as well as with levels of Tom40 expression in the mitochondria. Thus, we conclude that the TOM complex participates
in O2•− release from mitochondria. 相似文献
6.
Bhushan S Kumar A Malik F Andotra SS Sethi VK Kaur IP Taneja SC Qazi GN Singh J 《Apoptosis : an international journal on programmed cell death》2007,12(10):1911-1926
A triterpenediol (TPD) comprising of isomeric mixture of 3α, 24-dihydroxyurs-12-ene and 3α, 24-dihydroxyolean-12-ene from
Boswellia serrata induces apoptosis in cancer cells. An attempt was made in this study to investigate the mechanism of cell death by TPD in
human leukemia HL-60 cells. It inhibited cell proliferation with IC50 ∼ 12 μg/ml and produced apoptosis as measured by various biological end points e.g. increased sub-G0 DNA fraction, DNA ladder
formation, enhanced AnnexinV-FITC binding of the cells. Further, initial events involved massive reactive oxygen species (ROS)
and nitric oxide (NO) formation, which were significantly inhibited by their respective inhibitors. Persistent high levels
of NO and ROS caused Bcl-2 cleavage and translocation of Bax to mitochondria, which lead to loss of mitochondrial membrane
potential (Δψm) and release of cytochrome c, AIF, Smac/DIABLO to the cytosol. These events were associated with decreased expression of
survivin and ICAD with attendant activation of caspases leading to PARP cleavage. Furthermore, TPD up regulated the expression
of cell death receptors DR4 and TNF-R1 level, leading to caspase-8 activation. These studies thus demonstrate that TPD produces
oxidative stress in cancer cells that triggers self-demise by ROS and NO regulated activation of both the intrinsic and extrinsic
signaling cascades. 相似文献
7.
This study examined the impact of ceramide, an intracellular mediator of apoptosis, on the mitochondria to test the hypothesis
that ceramide utilized p38 MAPK in the mitochondria to alter mitochondrial potential and induce apoptosis. The capacity of
ceramide to adversely affect mitochondria was demonstrated by the significant loss of mitochondrial potential (ΔΨm), indicated by a J-aggregate fluorescent probe, after embryonic chick cardiomyocytes were treated with the cell permeable
ceramide analogue C2-ceramide. p38 MAPK was identified in the mitochondrial fraction of the cell and p38 MAPK phosphorylation in this mitochondrial
fraction of the cell occurred with ceramide treatment. In addition, SAPK phosphorylation and a decrease in ERK phosphorylation
occurred in whole cell lysates after ceramide treatment. The p38 MAPK inhibitor SB 202190 but not the MEK inhibitor PD 98059
significantly inhibited ceramide-induced apoptosis and loss of ΔΨm. These data suggest that p38 MAPK is present in the mitochondria and its activation by ceramide indicates local signaling
more directly coupled to the mitochondrial pathway in apoptosis. (Mol Cell Biochem 278: 39–51, 2005) 相似文献
8.
Brustovetsky T Antonsson B Jemmerson R Dubinsky JM Brustovetsky N 《Journal of neurochemistry》2005,94(4):980-994
Cleaved or truncated BID (tBID) is known to oligomerize both BAK and BAX. Previously, BAK and BAX lacing the C-terminal fragment (BAXDeltaC) were shown to induce modest cytochrome c (Cyt c) release from rat brain mitochondria when activated by tBID. We now show that tBID plus monomeric full-length BAX induce extensive release of Cyt c, Smac/DIABLO, and Omi/HtrA2 (but not endonuclease G and the apoptosis inducing factor) comparable to the release induced by alamethicin. This occurs independently of the permeability transition without overt changes in mitochondrial morphology. The mechanism of the release may involve formation of reactive oxygen species (ROS) and activation of calcium-independent phospholipase A(2) (iPLA(2)). Indeed, increased ROS production and activated iPLA(2) were observed prior to massive Cyt c release. Furthermore, the extent of inhibition of Cyt c release correlated with the degree of suppression of iPLA(2) by the inhibitors propranolol, dibucaine, 4-bromophenacyl bromide, and bromenol lactone. Consistent with a requirement for iPLA(2) in Cyt c release from brain mitochondria, synthetic liposomes composed of lipids mimicking the outer mitochondrial membrane (OMM) but lacing iPLA(2) failed to release 10 kDa fluorescent dextran (FD-10) in response to tBID plus BAX. We propose that tBID plus BAX activate ROS generation, which subsequently augments iPLA(2) activity leading to changes in the OMM that allow translocation of certain mitochondrial proteins from the intermembrane space. 相似文献
9.
Agu Laisk Eero Talts Vello Oja Hillar Eichelmann Richard B. Peterson 《Photosynthesis research》2010,103(2):79-95
Fast cyclic electron transport (CET) around photosystem I (PS I) was observed in sunflower (Helianthus annuus L.) leaves under intense far-red light (FRL) of up to 200 μmol quanta m−2 s−1. The electron transport rate (ETR) through PS I was found from the FRL-dark transmittance change at 810 and 950 nm, which
was deconvoluted into redox states and pool sizes of P700, plastocyanin (PC) and cytochrome f (Cyt f). PC and P700 were in
redox equilibrium with K
e = 35 (ΔE
m = 90 mV). PS II ETR was based on O2 evolution. CET [(PS I ETR) − (PS II ETR)] increased to 50–70 μmol e− m−2 s−1 when linear electron transport (LET) under FRL was limited to 5 μmol e− m−2 s−1 in a gas phase containing 20–40 μmol CO2 mol−1 and 20 μmol O2 mol−1. Under these conditions, pulse-saturated fluorescence yield F
m was non-photochemically quenched; however, F
m was similarly quenched when LET was driven by low green or white light, which energetically precluded the possibility for
active CET. We suggest that under FRL, CET is rather not coupled to transmembrane proton translocation than the CET-coupled
protons are short-circuited via proton channels regulated to open at high ΔpH. A kinetic analysis of CET electron donors and
acceptors suggests the CET pathway is that of the reversed Q-cycle: Fd → (FNR) → Cyt cn → Cyt bh → Cyt bl → Rieske FeS → Cyt f → PC → P700 →→ Fd. CET is activated when PQH2 oxidation is opposed by high ΔpH, and ferredoxin (Fd) is reduced due to low availability of e− acceptors. The physiological significance of CET may be photoprotective, as CET may be regarded as a mechanism of energy
dissipation under stress conditions. 相似文献
10.
Fei Ma Xiao-Bo Chen Min Sang Peng Wang Jian-Ping Zhang Liang-Bi Li Ting-Yun Kuang 《Photosynthesis research》2009,100(1):19-28
We have attempted to investigate the correlation between the detergent-perturbed structural integrity of the Cyt b
6
f complex from the marine green alga Bryopsis corticulans and its photo-protective properties, for which the nonionic detergents n-octyl-β-d-glucopyranoside (β-OG) and n-dodecyl-β-d-maltoside (β-DM), respectively, were used for the preparation of Cyt b
6
f, and the singlet oxygen (1O2*) production as well as the triplet excited-state chlorophyll a (3Chl a*) formation and deactivation were examined by spectroscopic means. Near-infrared luminescence of 1O2
* (~1,270 nm) on photo-irradiation was detected for the β-OG preparation where the complex is mainly in oligomeric state, but
not for the β-DM one in which the complex exists in dimeric form. Under anaerobic condition, photo-excitation of Chl a in the β-DM preparation generated 3Chl a* with a lower quantum yield of ΦT ~ 0.02 and a longer lifetime of ~600 μs with respect to those as in the case of β-OG preparation, ΦT ~ 0.12 and 200–300 μs. These results prove that the enzymatically active and intact Cyt b
6
f complex on photo-excitation tends to produce little 3Chl a* or 1O2
*, which implies that the pigment–protein assembly of Cyt b
6
f complex per se is crucial for photo-protection.
F. Ma and X.-B. Chen contributed equally to this work. 相似文献
11.
Jesús M. Mercado F. Javier L. Gordillo F. Xavier Niell Félix L. Figueroa 《Journal of applied phycology》1999,11(5):455-461
Photosynthesis and cell composition of Porphyraleucosticta discs grown at low (< 0.0001% in air), current (control) and high (1% CO2 in air)inorganic carbon (Ci) concentrations were analyzed. Carbohydrate content in discs grown at high Ci increased (15.1 mg g-1 FW) with respect to the control (6.4 mg g FW-1), whereas soluble protein content decreased to one-third (5.6 to2.1 mg g-1 FW). Carbohydrate content was unaffected and soluble protein slightly increased in discs grown at low Ci. As a consequence of these changes, a lower C/N molar ratio (8.6) was found in the discs grown at low compared to high Ci(12.4). Nitrate reductase activity increased at high Ci from 0.3 ± 0.2 to 1.7 ± 0.4 μmolNO2
- g-1 FW h-1indicating that reduction and assimilation of nitrate were uncoupled. The response of photosynthesis to increasing irradiance,
estimated from O2evolution vs. irradiance curves, was affected by the treatments. Maximum quantum yield (Φ
O2°) and effective quantum yield (Φ
O2) at 150 μmol photon m-2s-1 decreased by 20% and 50%, respectively, at low Ci. These differences could be due to changes in photosynthetic electron flow between PSII and PSI. Treatments also produced
changes in maximal (Fv/Fm) and effective (ΔF/Fm′)quantum yield for photosystem II charge separation.
This revised version was published online in August 2006 with corrections to the Cover Date. 相似文献
12.
This work aimed to evaluate if gas exchange and PSII photochemical activity in maize are affected by different irradiance
levels during short-term exposure to elevated CO2. For this purpose gas exchange and chlorophyll a fluorescence were measured on maize plants grown at ambient CO2 concentration (control CO2) and exposed for 4 h to short-term treatments at 800 μmol(CO2) mol−1 (high CO2) at a photosynthetic photon flux density (PPFD) of either 1,000 μmol m−2 s−1 (control light) or 1,900 μmol m−2 s−1 (high light). At control light, high-CO2 leaves showed a significant decrease of net photosynthetic rate (P
N) and a rise in the ratio of intercellular to ambient CO2 concentration (C
i/C
a) and water-use efficiency (WUE) compared to control CO2 leaves. No difference between CO2 concentrations for PSII effective photochemistry (ΦPSII), photochemical quenching (qp) and nonphotochemical quenching (NPQ) was detected. Under high light, high-CO2 leaves did not differ in P
N, C
i/C
a, ΦPSII and NPQ, but showed an increase of WUE. These results suggest that at control light photosynthetic apparatus is negatively
affected by high CO2 concentration in terms of carbon gain by limitations in photosynthetic dark reaction rather than in photochemistry. At high
light, the elevated CO2 concentration did not promote an increase of photosynthesis and photochemistry but only an improvement of water balance due
to increased WUE. 相似文献
13.
Schlittenhardt D Schmiedt W Bonaterra GA Metz J Kinscherf R 《Cell and tissue research》2005,322(3):425-435
Apoptotic and inflammatory processes occur in human arteriosclerotic lesions. We examined the hypothesis whether both processes
are possibly associated by studying the colocalization of corresponding markers. In 11 human arteriosclerotic carotid arteries,
proapoptotic markers (CPP32 (caspase-3), poly(ADP-ribose) polymerase, apoptosis-inducing factor, c-Jun/AP-1, and p53) and proinflammatory markers (macrophage migration inhibitory factor (MIF) and cyclooxygenase-2) were found in macrophages
(MΦ) evaluated by computer-assisted immunohistomorphometry. Double-labeling studies demonstrated a colocalization of, both,
proapoptotic and proinflammatory markers in these MΦ. Moreover, these MΦ also contained oxidized low-density lipoproteins
(oxLDL). Exposure of cultured human MΦ to oxLDL, C6-ceramide, and tumor necrosis factor-alpha or H2O2 resulted in a significant increase of the apoptosis rate as well as of the MIF protein expression. Our study of MΦ in arteriosclerotic
carotid arteries and in vitro experiments provide evidence that markers of apoptosis and inflammation are not only significantly
increased but are also coexpressed. We conclude there are reciprocal modulatory interactions between apoptotic and inflammatory
pathways in human plaque MΦ, which might importantly modify plaque progression or stability.
J. Metz and R. Kinscherf are senior authors. 相似文献
14.
Veluthakal R Palanivel R Zhao Y McDonald P Gruber S Kowluru A 《Apoptosis : an international journal on programmed cell death》2005,10(4):841-850
C2-ceramide, a cell permeable analogue of ceramide [CER] markedly reduced mitochondrial membrane potential [MMP] in insulin-secreting INS cells, which was followed by a significant accumulation of cytochrome c [Cyt c] into the cytosolic compartment. In a manner akin to CER, exposure of these cells to interleukin-1β [IL-1β] also resulted in reduction in MMP and cytosolic accumulation of Cyt c. Further, long-term exposure of these cells to either CER [but not its inactive analogue] or IL-1β caused a marked reduction in their metabolic viability. However, unlike IL-1β, which increased nitric oxide [NO] release, CER-treatment of INS cells had no effects of CER on NO release were demonstrable. Together, these findings suggest that CER-induced mitochondrial effects may not be mediated via iNOS gene expression and NO production. CER also activated an okadaic acid -sensitive protein phosphatase [CAPP] in the purified mitochondrial fraction, suggesting that CAPP might represent one of the target proteins for CER in the β cell mitochondria. Together, our findings suggest direct detrimental effects of CER on mitochondrial function in β cells leading to their dysfunction and demise via apoptosis. Moreover, our findings provide evidence for a potential difference in the mechanisms underlying CER- and IL-1β-induced mitochondrial defects and apoptotic demise of the effete β cell. 相似文献
15.
Gupthar A.S. Bhattacharya S. Basu T.K. 《World journal of microbiology & biotechnology》2000,16(7):613-616
The maximum specific growth rate (μmax) of an ethanolic D-xylose-fermenting yeast, Pichia stipitis, showing non-linear growth trends in batch culture, was calculated using the rate equation μ2 = (1/Δt) ln(x
2/x
1). The absolute error Δμ, affecting μ2, was derived using an equation given by Borzani (1994). Based on the assumption of linearity of growth curves between two
closest time points, the relation between the two rate formulae, μ1 = (1/xˉ)dx
t
/dt and μ2 = (1/Δt) ln(x
2/x
1) was established. In a particular condition, when μ1 = μ2, an equation has been developed, the roots of which are the specific growth rates at different time points.
This revised version was published online in July 2006 with corrections to the Cover Date. 相似文献
16.
To investigate how excess excitation energy is dissipated in a ribulose-1,5-bisphospate carboxylase/oxygenase activase antisense
transgenic rice with net photosynthetic rate (P
N) half of that of wild type parent, we measured the response curve of P
N to intercellular CO2 concentration (C
i), electron transport rate (ETR), quantum yield of open photosystem 2 (PS2) reaction centres under irradiation (Fv′/Fm′), efficiency of total PS2 centres (ΦPS2), photochemical (qP) and non-photochemical quenching (NPQ), post-irradiation transient increase in chlorophyll (Chl) fluorescence (PITICF), and
P700+ re-reduction. Carboxylation efficiency dependence on C
i, ETR at saturation irradiance, and Fv′/Fm′, ΦPS2, and qP under the irradiation were significantly lower in the mutant. However, NPQ, energy-dependent quenching (qE), PITICF, and P700+ re-reduction were significantly higher in the mutant. Hence the mutant down-regulates linear ETR and stimulates cyclic electron
flow around PS1, which may generate the ΔpH to support NPQ and qE for dissipation of excess excitation energy. 相似文献
17.
mCICR is required for As2O3-induced permeability transition pore opening and cytochrome c release from mitochondria 总被引:1,自引:0,他引:1
The permeability transition pore (PTP) is central for apoptosis by acting as a good candidate pathway for the release of Cyt. c and apoptosis induction factors (AIF). Arsenite induces apoptosis via a direct effect on PTP. To characterize the exact mechanism for arsenite induces PTP opening, the effect of Ca2+ on As2O3-induced PTP opening, the relationship between As2O3-induced PTP opening and Cyt. c release from mitochondria and calcium-induced calcium release from mitochondria (mCICR), and the effects of As2O3 on Ca2+-induced PTP opening were studied. The results showed As2O3 induces Cyt. c release by triggering PTP opening. Ca2+ is necessary for As2O3-induced PTP opening. As2O3-induced PTP opening and Cyt. c release depends on mCICR. As2O3 promotes PTP opening by lowering Ca2+-threshold. These results indicated As2O3 induce Cyt. c release from mitochondria by lowering Ca2+-threshold for PTP and triggering mCICR-dependent PTP opening. Suggesting that it is possible to control apoptosis by altering Ca2+ threshold and mCICR to modulate PTP opening and Cyt. c release. 相似文献
18.
Photosynthesis of lichen symbiotic alga Trebouxia erici as affected by irradiance and osmotic stress
The relation between oxygen evolution rate (OER) and quantum yield of photochemical reactions in photosystem 2 (ΦPS2) was examined in lichen symbiotic alga Trebouxia erici Ahmadjian (strain UTEX 911) exposed to different irradiances and osmotic stress (2 M sucrose for 60 h). Linear relationship
was found between OER and ΦPS2 in control cell suspension within irradiance range of 0 – 500 μmol m−2 s−1. Under osmotic stress, OER and ΦPS2 were significantly reduced. Relation between OER and ΦPS2 was curvilinear due to strong osmotically-induced inhibition of OER at high irradiance. The highest used irradiance (500
μmol m−2 s−1) was photoinhibitory for osmotically-stressed T. erici because non-photochemical quenching (NPQ) increased substantially. Energy-dependent quenching represented major part of NPQ
increase. Osmotic stress led also to the reduction of capacity of photochemical processes in PS 2 (FV/FM) and increase in F0/FM. These changes indicated negative effects of osmoticum on structure and function of photosynthetic apparatus. 相似文献
19.
20.
Mitochondrial release of pro-apoptotic proteins: electrostatic interactions can hold cytochrome c but not Smac/DIABLO to mitochondrial membranes 总被引:8,自引:0,他引:8
Uren RT Dewson G Bonzon C Lithgow T Newmeyer DD Kluck RM 《The Journal of biological chemistry》2005,280(3):2266-2274
A key step in the initiation of apoptosis is the release from the mitochondrial intermembrane space of cytochrome c and other pro-apoptotic proteins such as Smac/DIABLO, Omi/HtrA2, apoptosis-inducing factor (AIF), and endonuclease G (EndoG). Discrepancies have arisen, however, as to whether all these proteins are released in different systems. Our results suggest that failure to observe cytochrome c release may be due to the use of different buffers because after permeabilization by caspase-8 cleaved human Bid (tBid), cytochrome c dissociation from mitochondria was highly dependent on ionic strength and required 50-80 mm KCl, NaCl, or LiCl. In addition, mitochondria isolated from apoptotic cells using low ionic strength buffer bound a greater proportion of endogenous cytochrome c. In contrast to cytochrome c, Smac/DIABLO and Omi/HtrA2 were released independent of ionic strength, and AIF and EndoG behaved as if they are exposed to the intermembrane space but tethered to or within the inner membrane. AIF and EndoG were also not released by active caspases, which suggests their involvement in apoptosis may be limited. In summary, whereas tBid permeabilizes the outer membrane to cytochrome c, Smac/DIABLO, and Omi/HtrA2, the release of cytochrome c during apoptosis will be underestimated unless sufficient ionic strength is maintained to overcome the electrostatic association of cytochrome c with membranes. 相似文献