共查询到14条相似文献,搜索用时 15 毫秒
1.
Effects of myocardial ischemia and reperfusion on mitochondrial function and susceptibility to oxidative stress 总被引:8,自引:0,他引:8
We investigated the effects of ischemia duration on the functional response of mitochondria to reperfusion and its relationship
with changes in mitochondrial susceptibility to oxidative stress. Mitochondria were isolated from hearts perfused by the Langendorff
technique immediately after different periods of global ischemia or reperfusion following such ischemia periods. Rates of
O2 consumption and H2O2 release with complex I- and complex II-linked substrates, lipid peroxidation, overall antioxidant capacity, capacity to remove
H2O2, and susceptibility to oxidative stress were determined. The effects of ischemia on some parameters were time dependent so
that the changes were greater after 45 than after 20 min of ischemia, or were significantly different to the nonischemic control
only after 45 min of ischemia. Thus, succinate-supported state 3 respiration exhibited a significant decrease after 20 min
of ischemia and a greater decrease after 45 min, while pyruvate malate-supported respiration showed a significant decrease
only after 45 min of ischemia, indicating an ischemia-induced early inhibition of complex II and a late inhibition of complex
I. Furthermore, both succinate and pyruvate malate-supported H2O2 release showed significant increases only after 45 min of ischemia. Similarly, whole antioxidant capacity significantly increased
and susceptibility to oxidants significantly decreased after 45 min of ischemia. Such changes were likely due to the accumulation
of reducing equivalents, which are able to remove peroxides and maintain thiols in a reduced state. This condition, which
protects mitochondria against oxidants, increases mitochondrial production of oxyradicals and oxidative damage during reperfusion.
This could explain the smaller functional recovery of the tissue and the further decline of the mitochondrial function after
reperfusion following the longer period of oxygen deprivation.
Received 18 May 2001; received after revision 17 July 2001; accepted 24 July 2001 相似文献
2.
Thyroid hormone-induced oxidative stress 总被引:6,自引:0,他引:6
3.
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
4.
Summary Chronic daily intake of 0.5% H2O2 in drinking water decreased Se-dependent glutathione peroxidase (Se-GSHPx) activity in rat skeletal muscle, kidney and liver. Non-Se GSHPx activity decreased in kidney. Deprivation of drinking water decreased Se-GSHPx activity in kidney and non-Se GSHPx activity in kidney and liver. H2O2 intake decreased activity of catalase in rat skeletal muscle. H2O2 intake or water deprivation caused no changes in these enzyme activities in mice. 相似文献
5.
Melatonin regulation of antioxidant enzyme gene expression 总被引:15,自引:0,他引:15
Mayo JC Sainz RM Antoli I Herrera F Martin V Rodriguez C 《Cellular and molecular life sciences : CMLS》2002,59(10):1706-1713
Antioxidant enzymes (AOEs) are part of the primary cellular defense against free radicals induced by toxins and/or spontaneously
formed in cells. Melatonin (MLT) has received much attention in recent years due to its direct free radical scavenging and
antioxidant properties. In the present work we report that MLT, at physiological serum concentrations (≈ 1 nM), increases
the mRNA of both superoxide dismutases (SODs) and glutathione peroxidase (GPx) in two neuronal cell lines. The MLT effect
on both SODs and GPx mRNA was mediated by a de novo synthesized protein. MLT alters mRNA stability for Cu-Zn SOD and GPx.
Experiments with a short time treatment (pulse action) of MLT suggest that the regulation of AOE gene expression is likely
to be receptor mediated, because 1-h treatment with MLT results in the same response as a 24-h treatment.
Received 18 June 2002; received after revision 5 August 2002; accepted 27 August 2002
RID="*"
ID="*"Corresponding author. 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.
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
8.
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
9.
Dual role of endogenous nitric oxide in tumor necrosis factor shock: induced NO tempers oxidative stress 总被引:1,自引:0,他引:1
Cauwels A Bultinck J Brouckaert P 《Cellular and molecular life sciences : CMLS》2005,62(14):1632-1640
Tumor necrosis factor (TNF) is involved in pathologies like septic shock, inflammatory bowel disease and rheumatoid arthritis. TNF and lipopolysaccharide can incite lethal shock, in which cardiovascular collapse is centrally orchestrated by the vasodilating free radical nitric oxide (NO). However, NO synthase (NOS) inhibition causes increased morbidity and/or mortality, suggesting a dual role for NO. To investigate the potential protective role of NO during TNF shock, we treated mice with TNF with or without NOS inhibition. Experiments in endothelial- NOS- and inducible NOS-deficient mice identified inducible NOS as the source of protective NO. Distinctive TNF-induced lipid peroxidation, especially in liver and kidney, was aggravated by NOS inhibition. In addition, various antioxidant treatments and a phospholipase A2 (PLA2) inhibitor prevented sensitization by NOS inhibition. Together, these in vivo results indicate that induced NO not only causes hemodynamic collapse, but is also essential for curbing TNF-induced oxidative stress, which appears to hinge on PLA2-dependent mechanisms.Received 29 March 2005; received after revision 29 April 2005; accepted 24 May 2005 相似文献
10.
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
11.
Hydrogen peroxide and hydroxyl radical involvement in the activation of caspase-3 in chemically induced apoptosis of HL-60 cells 总被引:3,自引:0,他引:3
Kajiwara K Ikeda K Kuroi R Hashimoto R Tokumaru S Kojo S 《Cellular and molecular life sciences : CMLS》2001,58(3):485-491
Apoptosis of HL-60 cells induced by actinomycin D, H7, or daunorubicin was shown to involve the activation of caspase-3-like
protease, 2 h after the addition of these drugs, based on microassay of enzyme activity by high-performance liquid chromatography.
Catalase and a spin trap, N-t-butyl--phenylnitrone, which effectively inhibited the apoptosis induced by these drugs, also inhibited the activation of caspase-3-like
protease. These results suggest that hydrogen peroxide and the hydroxyl radical are common mediators of caspase-3 activation
caused by these chemicals, with apparently different functional mechanisms. Based on mitochondrial activity determined by
oxygen consumption, complexes I, II, and IV were inhibited by actinomycin D. H7 inhibited complexes I and IV, 1 and 1.5 h
respectively, after the addition of the drug to HL-60 cells. Daunorubicin inhibited complex IV, 1.5 h after the addition of
the drug to HL-60 cells. Inhibition of complex IV by actinomycin D, H7, and daunorubicin were almost fully restored by the
addition of cytochrome c. The release to the cytosol of cytochrome c by these drugs was also demonstrated by Western blot
analysis. Addition of catalase inhibited the depression of complex IV activity induced by actinomycin D and H7. These observations
indicate a direct relationship between hydrogen peroxide and the release of cytochrome c during apoptosis caused by actinomycin
D, H7, and daunorubicin.
Received 24 November 2000; received after revision 2 January 2001; accepted 30 January 2001 相似文献
12.
Brömme HJ Ebelt H Peschke D Peschke E 《Cellular and molecular life sciences : CMLS》1999,55(3):487-493
Depending on the availability of suitable reducing agents, alloxan can be either a prooxidant or an antioxidant. Alloxan
and its reduced derivative, dialuric acid, act as a redox couple, driven by reduced glutathione (GSH) or L-cysteine, generating
in vitro in the presence of oxygen, both superoxide radical and hydrogen peroxide. The production of superoxide radicals was
shown by the appearance of lucigenin chemiluminescence (CL) as well as by the generation of formazan from nitroblue tetrazolium
(NBT). The lucigenin CL as well as the NBT reduction was inhibited by superoxide dismutase and partially by catalase. Melatonin
inhibited alloxan-mediated CL. In contrast, in the absence of reducing agents, alloxan is a scavenger of superoxide radicals
formed by other reactions. Because of the high content of reducing compounds in the cell (e.g. glutathione), it is suggested
that alloxan acts in vivo mainly as a generator of reactive oxygen species.
Received 9 November 1998; received after revision 15 January 1999; accepted 15 January 1999 相似文献
13.
P. A. Parsons 《Cellular and molecular life sciences : CMLS》1996,52(7):643-646
Life span and development time are considered in the context of the abiotic stresses to which free-living organisms are normally exposed. Under these circumstances, long life span depends upon metabolically efficient stress-resistance genes, which tend to be heterozygous. Similarly, rapid development time tends to be a feature of heterozygous stress-resistant individuals. Therefore, individuals who have high inherited stress resistance should develop fastest and live longest; in addition, they should show high homeostasis in the face of the energy costs of stress. In this way, the stress theory of aging can incorporate the developmental stage, based upon oxidative stress as an important major direct challenge. 相似文献
14.
Summary Wistar rats show a circadian variation in their response to stress. Pinealectomy exacerbates stress-induced gastric ulceration in rats. This effect is counteracted by melatonin administration. 相似文献