共查询到11条相似文献,搜索用时 15 毫秒
1.
Functional and biochemical characteristics of mitochondrial fractions from rat liver in cold-induced oxidative stress 总被引:2,自引:0,他引:2
Venditti P De Rosa R Caldarone G Di Meo S 《Cellular and molecular life sciences : CMLS》2004,61(24):3104-3116
We determined characteristics of rat liver mitochondrial fractions, resolved at 1000 (M1), 3000 (M3), and 10,000 g (M10) after 2 and 10 days cold exposure. In all groups, the M1 fraction exhibited the highest oxidative capacity, oxidative damage, H2O2 production rate, and susceptibility to stress conditions, and the lowest antioxidant levels. Cold exposure increased cytochrome oxidase activity in all fractions and succinate-supported O2 consumption in the M1 and M10 fractions during state 3 and state 4 respiration, respectively. With succinate, the H2O2 release rate increased in all fractions during state 4 and state 3 respiration, whereas with pyruvate/malate, it increased only during state 4 respiration. Increases in tissue mitochondrial proteins caused a faster H2O2 flow from the mitochondrial to cytosolic compartment, which was limited by the reduction in the M1 fraction. Despite increased liposoluble antioxidant levels, cold also caused enhanced oxidative damage and susceptibility to oxidative challenge and Ca2+-induced swelling in all fractions. These changes leading to elimination of H2O2-overproducing mitochondria avoided excessive tissue damage. We propose that triiodothyronine, whose levels increase in the cold environment, brings about the biochemical changes producing oxidative damage and those limiting its extent.Received 16 July 2004; received after revision 27 September 2004; accepted 18 October 2004 相似文献
2.
Role of nitric oxide in the functional response to ischemia-reperfusion of heart mitochondria from hyperthyroid rats 总被引:2,自引:0,他引:2
Venditti P De Rosa R Cigliano L Agnisola C Di Meo S 《Cellular and molecular life sciences : CMLS》2004,61(17):2244-2252
We investigated the role of nitric oxide (NO) in the mitochondrial derangement associated with the functional response to ischemia-reperfusion of hyperthyroid rat hearts. Mitochondria were isolated at 3000 g from hearts subjected to ischemia-reperfusion, with or without N-nitro-L-arginine (L-NNA, an NO synthase inhibitor). During reperfusion, hyperthyroid hearts displayed tachycardia and low functional recovery. Their mitochondria exhibited O2 consumption similar to euthyroid controls, while H2O2 production, hydroperoxide, protein-bound carbonyl and nitrotyrosine levels, and susceptibility to swelling were higher. L-NNA blocked the reperfusion tachycardic response and increased inotropic recovery in hyperthyroid hearts. L-NNA decreased mitochondrial H2O2 production and oxidative damage, and increased respiration and tolerance to swelling. Such effects were higher in hyperthyroid preparations. These results confirm the role of mitochondria in ischemia-reperfusion damage, and strongly suggest that NO overproduction is involved in the high mitochondrial dysfunction and the low recovery of hyperthyroid hearts from ischemia-reperfusion. L-NNA also decreased protein content and cytochrome oxidase activity of a mitochondrial fraction isolated at 8000 g. This and previous results suggest that the above fraction contains, together with light mitochondria, damaged mitochondria coming from the heaviest fraction, which has the highest cytochrome oxidase activity and capacity to produce H2O2. Therefore, we propose that the high mitochondrial susceptibility to swelling, favoring mitochondrial population purification from H2O2-overproducing mitochondria, limits hyperthyroid heart oxidative stress.Received 24 March 2004; received after revision 9 June 2004; accepted 5 July 2004 相似文献
3.
Hydrogen peroxide protects tobacco from oxidative stress by inducing a set of antioxidant enzymes 总被引:13,自引:0,他引:13
Gechev T Gadjev I Van Breusegem F Inzé D Dukiandjiev S Toneva V Minkov I 《Cellular and molecular life sciences : CMLS》2002,59(4):708-714
Tolerance against oxidative stress generated by high light intensities or the catalase inhibitor aminotriazole (AT) was induced
in intact tobacco plants by spraying them with hydrogen peroxide (H2O2). Stress tolerance was concomitant with an enhanced antioxidant status as reflected by higher activity and/or protein levels
of catalase, ascorbate peroxidase, guaiacol peroxidases, and glutathione peroxidase, as well as an increased glutathione pool.
The induced stress tolerance was dependent on the dose of H2O2 applied. Moderate doses of H2O2 enhanced the antioxidant status and induced stress tolerance, while higher concentrations caused oxidative stress and symptoms
resembling a hypersensitive response. In stress-tolerant plants, induction of catalase was 1.5-fold, that of ascorbate peroxidase
and glutathione peroxidase was 2-fold, and that of guaiacol peroxidases was approximately 3-fold. Stress resistance was monitored
by measuring levels of malondialdehyde, an indicator of lipid peroxidation. The levels of malondialdehyde in all H2O2-treated plants exposed to subsequent high light or AT stress were similar to those of unstressed plants, whereas lipid peroxidation
in H2O2-untreated plants stressed with either high light or AT was 1.5- or 2-fold higher, respectively. Although all stress factors
caused increases in the levels of reduced glutathione, its levels were much higher in all H2O2-pretreated plants. Moreover, significant accumulation of oxidized glutathione was observed only in plants that were not pretreated
with H2O2. Extending the AT stress period from 1 to 7 days resulted in death of tobacco plants that were not pretreated with H2O2, while all H2O2-pretreated plants remained little affected by the prolonged treatment. Thus, activation of the plant antioxidant system by
H2O2 plays an important role in the induced tolerance against oxidative stress.
Received 11 December 2001; received after revision 25 January 2002; accepted 4 February 2002 相似文献
4.
Thyroid hormone-induced oxidative stress 总被引:6,自引:0,他引:6
5.
Parihar MS Parihar A Fujita M Hashimoto M Ghafourifar P 《Cellular and molecular life sciences : CMLS》2008,65(7-8):1272-1284
α-Synuclein is a neuron-specific protein that contributes to the pathology of Parkinson’s disease via mitochondria-related mechanisms. The present study investigated possible interaction of α-synuclein with mitochondria and
consequences of such interaction. Using SHSY cells overexpressing α-synuclein A53T mutant or wild-type, as well as isolated
rat brain mitochondria, the present study shows that α-synuclein localizes at the mitochondrial membrane. In both SHSY cells
and isolated mitochondria, interaction of α-synuclein with mitochondria causes release of cytochrome c, increase of mitochondrial calcium and nitric oxide, and oxidative modification of mitochondrial components. These findings
suggest a pivotal role for mitochondria in oxidative stress and apoptosis induced by α-synuclein.
Received 27 December 2007; received after revision 7 February 2008; accepted 8 February 2008 相似文献
6.
Zhu X Su B Wang X Smith MA Perry G 《Cellular and molecular life sciences : CMLS》2007,64(17):2202-2210
Oxidative stress is one of the earliest events of Alzheimer disease (AD), with implications as an important mediator in the
onset, progression and pathogenesis of the disease. The generation of reactive oxygen species (ROS) and its consequent cellular
damage/response contributes to much of the hallmark AD pathology seen in susceptible neurons. The sources of ROS-mediated
damage appear to be multi-faceted in AD, with interactions between abnormal mitochondria, redox transition metals, and other
factors. In this review, we provide an overview of these potential causes of oxidative stress in AD. 相似文献
7.
Cancer cell metabolism is characterized by limited oxidative phosphorylation in order to minimize oxidative stress. We have
previously shown that the flavonoid flavone in HT-29 colon cancer cells increases the uptake of pyruvate or lactate into mitochondria,
which is followed by an increase in O2−.. production that finally leads to apoptosis. Similarly, a supply of palmitoylcarnitine in combination with carnitine induces
apoptosis in HT-29 cells by increasing the mitochondrial respiration rate. Here we show that flavone-induced apoptosis is
increased more than twofold in the presence of palmitoylcarnitine due to increased mitochondrial fatty acid transport and
the subsequent metabolic generation of O2−. in mitochondria is the initiating factor for the execution of apoptosis.
Received 12 August 2005; received after revision 12 October 2005; accepted 14 October 2005 相似文献
8.
Martínez Muñoz C Post JA Verkleij AJ Verrips CT Boonstra J 《Cellular and molecular life sciences : CMLS》2001,58(7):990-996
Activation of mitogen-activated protein (MAP) kinase is essential for cyclin D1 expression and provides a link between mitogenic
signalling and cell cycle progression. Hydrogen peroxide (H2 O2 ) activates MAP kinase; however, it is not known whether this leads to cyclin D expression. Sustained expression of cyclin
D1 and D2 was observed when Her14 fibroblasts were incu-bated with 3 mM or higher H2 O2 concentrations. Similar results were obtained when cells were incubated in the presence of serum (FCS). However, the sustained
expres-complex sion of cyclin D1 and D2 upon H2 O2 treatment was not due to the MAP kinase pathway, because MAP kinase kinase inhibitors did not inhibit cyclin D expression.
Furthermore, cyclin D1 and D2 levels remained constant even after addition of a protein synthesis inhibitor, indicating that
the effect of H2 O2 was not due to induction of protein synthesis. These results indicate that H2 O2 reversibly inhibits the ubiquitin-proteasome dependent degra-dation of cyclin D1 and D2, probably by transiently in-hibiting
ubiquitination and/or the proteasome.
Received 12 March 2001; received after revision 5 April 2001; accepted 9 April 2001 相似文献
9.
J. W. M. Lagerberg J. VanSteveninck T. M. A. R. Dubbelman 《Cellular and molecular life sciences : CMLS》1997,53(3):257-262
The fluorescent dye Merocyanine 540 (MC540) is often used as a probe to monitor the molecular packing of phospholipids in
the outer leaflet of biomembranes. In a previous study we showed that the increased staining of erythrocytes with a perturbed
membrane structure was mainly due to an increase in the fluorescence yield of cell-bound MC540, rather than to an increase
of the number of bound molecules. Erythrocytes and ghosts exposed to continuous fluxes of H2O2 exhibited pronounced lipid peroxidation. Further, red blood cells subjected to this form of oxidative stress also showed
increased staining with MC540. It appeared that this was caused by a strong increase in binding of MC540, together with a
slight red shift of the fluorescence emission maximum and a small increase in the fluorescence yield of bound MC540. The changed
MC540 binding characteristics were not observed when lipid peroxidation was suppressed by the presence of the antioxidant
BHT in the incubation medium. However, open ghosts exposed to H2O2 showed no increase of MC540 binding, excluding a direct involvement of lipid peroxidation. Measurement of fluorescence emission
spectra and gel filtration studies showed that MC540 can bind to H2O2-exposed hemoglobin. Experiments with erythrocytes lysed in hypotonic medium after exposure to H2O2 revealed that peroxidation of lipids with H2O2 induced a non-specific permeabilization of the plasma membrane to MC540, thereby allowing MC540 to bind to the oxidatively
denatured, more hydrophobic hemoglobin. These results indicate that conclusions about packing of phospholipids in the outer
leaflet of the membrane based on increased MC540-staining should be drawn with care.
Received 27 September 1996; received after revision 5 November 1996; accepted 27 November 1996 相似文献
10.
氧化酪蛋白对小鼠组织抗氧化能力及血液肽组成的影响 总被引:1,自引:0,他引:1
目的研究酪蛋白经过加热氧化和脂质过氧化物MDA氧化后,对小鼠体内氧化还原状态及小鼠血液中肽组成的影响。方法酪蛋白经100℃加热(0、30、60、90min)和丙二醛(MDA)氧化(MDA终浓度0、0.2、20、200mmol/L)处理,测定其羰基、巯基含量及表面疏水性的变化。小鼠分为四组,分别灌胃生理盐水、正常酪蛋白、加热90rain、MDA氧化酪蛋白,测定0、30、60、90、120、160min血液中自由基水平,并采用HPLC-MS分析灌胃后120min小鼠血浆肽组分的变化,测定小鼠的肝脏、空肠、十二指肠组织抗氧化能力指标(总抗氧化能力T—AOC、丙二醛MDA、还原型谷胱甘肽GSH)。结果酪蛋白经过两种氧化处理,羰基含量均随氧化程度呈显著上升,巯基含量呈下降趋势。加热氧化后酪蛋白表面疏水性比正常酪蛋白低,而MDA氧化导致疏水性上升。小鼠血液中自由基最高峰出现在灌胃后160min。灌胃两种方式处理的酪蛋白,血液中自由基的含量均显著高于灌胃正常酪蛋白组(P〈0.05),肝脏、空肠、十二指肠还原型谷胱甘肽(GSH)含量和总抗氧化能力(T-AOC)均低于正常酪蛋白组,丙二醛(MDA)含量显著提高(P〈0.05)。HPLC—MS分析显示,灌胃MDA氧化酪蛋白组血液中肽组成与对照组不同,出现c7H15N4O含羰基类的物质:结论氧化会导致酪蛋白理化性质的改变,摄入氧化酪蛋白引起机体的氧化应激,降低组织抗氧化能力。 相似文献
11.
Summary In vitro applications of juvenile hormone III and a juvenile hormone analogue, methoprene, were made to mitochondria isolated from dorsal longitudinal flight muscles of adultLocusta migratoria L. Both compounds completely inhibited oxygen consumption at the highest concentrations used. At lower concentrations, state 3 respiration and respiratory control were reduced but the ADP/O ratio was largely unaffected. 相似文献