共查询到20条相似文献,搜索用时 15 毫秒
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J Liu H C Yeo E Overvik-Douki T Hagen S J Doniger D W Chyu G A Brooks B N Ames D W Chu 《Journal of applied physiology》2000,89(1):21-28
The responses to oxidative stress induced by chronic exercise (8-wk treadmill running) or acute exercise (treadmill running to exhaustion) were investigated in the brain, liver, heart, kidney, and muscles of rats. Various biomarkers of oxidative stress were measured, namely, lipid peroxidation [malondialdehyde (MDA)], protein oxidation (protein carbonyl levels and glutamine synthetase activity), oxidative DNA damage (8-hydroxy-2'-deoxyguanosine), and endogenous antioxidants (ascorbic acid, alpha-tocopherol, glutathione, ubiquinone, ubiquinol, and cysteine). The predominant changes are in MDA, ascorbic acid, glutathione, cysteine, and cystine. The mitochondrial fraction of brain and liver showed oxidative changes as assayed by MDA similar to those of the tissue homogenate. Our results show that the responses of the brain to oxidative stress by acute or chronic exercise are quite different from those in the liver, heart, fast muscle, and slow muscle; oxidative stress by acute or chronic exercise elicits different responses depending on the organ tissue type and its endogenous antioxidant levels. 相似文献
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Lushchak VI Bagnyukova TV 《Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology》2007,148(4):390-397
The effects of hypoxia (0.4 mg O2/L) for 2, 6 or 10 h and subsequent normoxic recovery on the levels of lipid peroxides, thiobarbituric acid reactive substances, protein carbonyls (CP), free thiols, and the activities of six antioxidant and associated enzymes were measured in the brain, liver, and skeletal muscle of the rotan Perccottus glenii. Hypoxia increased CP content in the brain (5.0–7.4-fold), liver (2.2–3.3-fold) and muscle (3.2–61-fold) relative to controls and the levels remained elevated during recovery. Lipid peroxide content rose within 2 h of hypoxia in all tissues examined with the most marked increase (8.7-fold) in the liver, but decreased again during longer hypoxic exposure except in the muscle. Levels of low-molecular mass thiols were transiently lowered after 2 h hypoxia in all tissues, but were higher compared with controls after longer hypoxic exposure and recovery. Hypoxia decreased protein thiol content in the liver and muscle that return to control levels during recovery. Experimental conditions affected enzyme activities in a different manner. Superoxide dismutase activity rose two-fold in the liver of hypoxic fish, and a similar tendency was seen in muscle glutathione-S-transferase. Activities of other enzymes were decreased or unchanged during hypoxia and elevated in some cases during normoxic recovery. Taken together, these data show that hypoxia resulted in the development of oxidative stress and a compensatory changes of antioxidant enzymes in the tissues. 相似文献
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Neuronal Mitochondrial Toxicity of Malondialdehyde: Inhibitory Effects on Respiratory Function and Enzyme Activities in Rat Brain Mitochondria 总被引:1,自引:0,他引:1
Jiangang Long Changsheng Liu Lijuan Sun Hongxiang Gao Jiankang Liu 《Neurochemical research》2009,34(4):786-794
Malondialdehyde (MDA) is a product of oxidative damage to lipids, amino acids and DNA, and accumulates with aging and diseases.
MDA can possibly react with amines so as to modify proteins and inactivate enzymes; it can also modify nucleosides so as to
cause mutagenicity. Brain mitochondrial dysfunction is a major contributor to aging and neurodegenerative diseases. We hypothesize
that MDA accumulated during aging targets mitochondrial enzymes so as to cause further mitochondrial dysfunction and additional
contributions to aging and neurodegeneration. Herein, we investigated the neuronal mitochondrial toxic effects of MDA on mitochondrial
respiration and activities of enzymes (mitochondrial complexes I–V, α-ketoglutarate dehydrogenase (KGDH) and pyruvate dehydrogenase
(PDH)), in isolated rat brain mitochondria. MDA depressed mitochondrial membrane potential, and also showed a dose-dependent
inhibition of mitochondrial complex I- and complex II-linked respiration. Complex I and II, and PDH activities were depressed
by MDA at ≥0.2 μmol/mg; KGDH and complex V were inhibited by ≥0.4 and ≥1.6 μmol MDA/mg, respectively. However, MDA did not
have any toxic effects on complex III and IV activities over the range 0–2 μmol/mg. MDA significantly elevated mitochondrial
reactive oxygen species (ROS) and protein carbonyls at 0.2 and 0.002 μmol/mg, respectively. As for the antioxidant defense
system, a high dose of MDA slightly decreased mitochondrial GSH and superoxide dismutase. These results demonstrate that MDA
causes neuronal mitochondrial dysfunction by directly promoting generation of ROS and modifying mitochondrial proteins. The
results suggest that MDA-induced neuronal mitochondrial toxicity may be an important contributing factor to brain aging and
neurodegenerative diseases.
Special issue article in honor of Dr. Akitane Mori. 相似文献
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为探讨低温对机体能量代谢、器官/组织抗氧化能力和过氧化自由基水平的影响及其内在联系,本研究测定了不同时间低温和梯度低温处理的黑线仓鼠的摄食量、体重、主要内脏器官/组织的过氧化物歧化酶(SOD)、过氧化氢酶(CAT)、H2O2和丙二醛(MDA)水平。低温使摄食量显著增加,但未影响体重。低温暴露42 d使心脏和骨骼肌MDA水平、骨骼肌SOD活性显著升高;梯度低温使脑和肾脏H2O2水平、肝脏和骨骼肌SOD活性显著降低,使脑、肝脏、肺、肾脏MDA水平、脑和小肠SOD活性显著升高。抗氧化能力和过氧化自由基水平在不同器官之间相关性存在差异,同一器官内二者的相关性在肾脏为100%,肝脏66.7%,骨骼肌50.0%。结果表明:(1)过氧化自由基的产生与低温暴露的时间和程度有关;(2)不同器官/组织过氧化自由基水平不同;(3)部分器官/组织抗氧化酶活性的变化与过氧化自由基水平的变化密切相关,可能是防止过氧化损伤的主要防御系统。 相似文献
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C. Feillet-Coudray T. Sutra G. Fouret J. Ramos C. Wrutniak-Cabello G. Cabello J.P. Cristol C. Coudray 《Free radical biology & medicine》2009,46(5):624-632
Mitochondrial and NADPH oxidase systems and oxidative stress were investigated in 12 week high-fat high-sucrose (HFHS) diet-fed rats. A protective effect of wine polyphenol (PP) extract was also examined. In liver, maximal activities of CII and CII+III mitochondrial complexes were decreased but NADPH oxidase expression (p22phox and p47phox) and NADPH oxidase-dependent superoxide anion production were not modified, whereas oxidative stress (lipid and protein oxidation products and antioxidant systems) was increased with HFHS diet. In muscle, anion superoxide production was slightly increased while mitochondrial complex activities and lipid and protein oxidation products were not modified with HFHS diet. In heart, NADPH oxidase expression and superoxide anion production were increased, and maximal activity of mitochondrial respiratory chain complexes or oxidative stress parameters were not modified. Wine polyphenol extract had an inhibiting effect on liver oxidative stress and on heart NADPH oxidase expression and superoxide anion production, and on induction of hepatic steatosis with HFHS diet. Induction of mitochondrial dysfunction could be a primary event in the development of oxidative stress in liver, while in skeletal muscle and in heart the NADPH oxidase system seems to be mainly involved in oxidative stress. Wine polyphenol extract was shown to partially prevent oxidative stress in liver and heart tissues and to nearly completely prevent steatosis development in liver. 相似文献
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Folic acid (FA), is a group B vitamin, has high reactive oxygen radicals quenching ability, resulting in protection against oxidative damage in aerobic cell. Acetaminophen (N-acetyl-p-aminophenol, APAP) is a nonsteroidal anti-inflammatory drug, and can promote oxidative damage in liver and kidney tissues. The aim of this study was to investigate whether folic acid has protective effects on oxidative liver and kidney injury caused by experimental APAP toxication. Forty female Sprague dawley rats were divided into 5 groups; control, APAP, FA, APAP+FA, and APAP+N-acetylcysteine (NAC) groups. APAP toxication was induced by oral gavage (3 g/kg bodyweight). FA (20 mg/kg bodyweight) and NAC (150 mg/kg bodyweight) were given by oral gavage to the specified groups. Oxidant and antioxidant parameter were determined in liver and kidney tissues. In addition, the liver and kidney tissues were histological evaluated. When compared with APAP group, superoxide dismutase (SOD) and catalase activities and glutathione levels were statistically higher, malondialdehyde (MDA) level and myeloperoxidase activity (except liver tissue) were statistically lower in both APAP+FA and APAP+NAC. Liver and kidney MDA level and kidney SOD activity were significantly lower in APAP+NAC group compared with APAP+FA group. Co-administration of NAC with APAP was found to provide protection, but hepatic cords were defective in some places and some glomerular tubules also had dilatation. Necrotic areas was reduced in the liver and the glomerular structure was in good condition in the APAP+FA group. As a result, FA might have a protective effect against APAP-induced hepato-nephrotoxicity and oxidative stress in rat. 相似文献
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S M Davies A Poljak M W Duncan G A Smythe M P Murphy 《Free radical biology & medicine》2001,31(2):181-190
Mitochondrial bioenergetic function is often reported to decline with age and the accumulation of oxidative damage is thought to contribute. However, there are considerable uncertainties about the amount and significance of mitochondrial oxidative damage in aging. We hypothesized that, as radical production in mitochondria is greater than the rest of the cell, protein oxidative damage should accumulate more in mitochondria than the cytoplasm, and that this relative accumulation should increase with age. To test these hypotheses we measured the accumulation of three markers of protein oxidative damage in liver, brain, and heart from young and old rats. Ortho- and meta-tyrosine levels in protein hydrolysates were measured by a gas chromatography/mass spectrometry assay, and protein carbonyl content was determined by ELISA. Using these assays we found no evidence for increased protein oxidative damage in mitochondria relative to the cytosol. Most increases found in protein oxidative damage on aging were modest for all three tissues and there was no consistent pattern of increased oxidative damage in mitochondrial proteins on aging. Mitochondrial oxidative phosphorylation complex activities were also assessed revealing 39-42% decreases in F0F1--ATP synthase activity in liver and heart on aging, but not in other oxidative phosphorylation complexes. These findings have implications for the contribution of mitochondrial oxidative damage and dysfunction to aging. 相似文献
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Mitochondrial involvement in Parkinson's disease, Huntington's disease, hereditary spastic paraplegia and Friedreich's ataxia 总被引:14,自引:0,他引:14
Schapira AH 《Biochimica et biophysica acta》1999,1410(2):159-170
Respiratory chain dysfunction has been identified in several neurodegenerative disorders. In Friedreich's ataxia (FA) and Huntington's disease (HD), where the respective mutations are in nuclear genes encoding non-respiratory chain mitochondrial proteins, the defects in oxidative phosphorylation are clearly secondary. In Parkinson's disease (PD) the situation is less clear, with some evidence for a primary role of mitochondrial DNA in at least a proportion of patients. The pattern of the respiratory chain defect may provide some clue to its cause; in PD there appears to be a selective complex I deficiency; in HD and FA the deficiencies are most severe in complex II/III with a less severe defect in complex IV. Aconitase activity in HD and FA is severely decreased in brain and muscle, respectively, but appears to be normal in PD brain. Free radical generation is thought to be of importance in both HD and FA, via excitotoxicity in HD and abnormal iron handling in FA. The oxidative damage observed in PD may be secondary to the mitochondrial defect. Whatever the cause(s) and sequence of events, respiratory chain deficiencies appear to play an important role in the pathogenesis of neurodegeneration. The mitochondrial abnormalities induced may converge on the function of the mitochondrion in apoptosis. This mode of cell death is thought to play an important role in neurodegenerative diseases and it is tempting to speculate that the observed mitochondrial defects in PD, HD and FA result directly in apoptotic cell death, or in the lowering of a cell's threshold to undergo apoptosis. Clarifying the role of mitochondria in pathogenesis may provide opportunities for the development of treatments designed to reverse or prevent neurodegeneration. 相似文献
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Benjamin Rey Marion Spée Maud Belouze Aurélie Girard Josiane Prost Damien Roussel Claude Duchamp 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》2010,180(2):239-246
At hatching, breaking eggshell induces a surge in oxygen availability that is likely to generate oxidative stress in newborn
chicks. To investigate the involvement of potential adaptive antioxidant mechanisms, we explored some markers of oxidative
stress and the regulation of muscle avian uncoupling protein (avUCP) and adenine nucleotide translocase (ANT) in ducklings
in the peri-hatching period. When compared with pre-hatching levels, the amount of peroxidized lipids were increased 24 h
after external pipping in gastrocnemius muscle (+37%) and heart (+39%) as well as the muscle avUCP mRNA expression (+60%)
but the susceptibility of red blood cells to free radicals (a functional test of oxidative status) was not affected. In order
to relate these changes to the oxidative transition of hatching, an imposed hypoxia/re-oxygenation protocol was used. Hatched
chicks that had spent the last 24 h of incubation in artificial severe hypoxia showed a rise in muscle (+50%) and heart (+69%)
lipid peroxidation, an increased susceptibility of red blood cells to free radicals, a marked over-expression of avUCP mRNA
(+105%) and a rise in mitochondrial ANT content (+54%). These results suggest that avian UCP and ANT may contribute to prepare
incubating eggs to the oxidative stress generated by the hypoxia/re-oxygenation transition naturally occurring at hatching. 相似文献
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José Pablo Vázquez-Medina Robert Elsner 《Journal of experimental marine biology and ecology》2007,345(2):110-118
Ischemia/reperfusion is a potentially hazardous condition that increases reactive oxygen species (ROS) production and oxidative damage. Seals of the phocid family experience repetitive episodes of ischemia/reperfusion during and after a dive as a consequence of preferential distribution of blood flow to the central nervous system and reduction or elimination of perfusion in most vascular beds. Previous studies showed that ROS production is higher in ringed seal than in domestic pig tissues as a direct consequence of the ischemia/reperfusion associated with the diving response; however, oxidative damage is not related to this high ROS production. Apparently, antioxidant enzyme activities participate in the antioxidant protection in ringed seal tissues. In the present study we addressed the potential antioxidant protection of the glutathione system against dive-induced ischemia/reperfusion in ringed seal tissues. Total glutathione (GSH-Eq = GSH + 2GSSG), glutathione (GSH) and glutathione disulfide (GSSG), the ratio GSSG:GSH-Eq, the activities of the enzymes glutathione disulfide reductase (GR) and glucose-6-phosphate dehydrogenase (G6PDH), as well as lipid peroxidation (TBARS) and carbonyl proteins, were measured in ringed seal and domestic pig heart, kidney, liver, lung and muscle samples. In heart, kidney, lung and muscle GSH-Eq and GSH content was higher in seal than in pig (p < 0.05). GSSG content was higher in seal than in pig heart kidney, liver and muscle (p < 0.05). GR and G6PDH activities were higher in all seal than in pig tissues (p < 0.05). GSSG:GSH-Eq ratio was higher in pig than in seal heart, and lung (p < 0.05). TBARS content was higher in pig than in seal lung (p < 0.05). Higher content of carbonyl proteins was present in pig than in seal heart, kidney, liver and muscle (p < 0.05). These results suggest that the glutathione levels and the activity of enzymes involved in its recycling are efficient mechanisms that ameliorate protein and lipid oxidative damage and protect ringed seal tissues against dive-induced ischemia/reperfusion. 相似文献
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Bruno Chausse Marcel A. Vieira-Lara Angélica B. Sanchez Marisa H. G. Medeiros Alicia J. Kowaltowski 《PloS one》2015,10(3)
Intermittent fasting (IF) is a dietary intervention often used as an alternative to caloric restriction (CR) and characterized by 24 hour cycles alternating ad libitum feeding and fasting. Although the consequences of CR are well studied, the effects of IF on redox status are not. Here, we address the effects of IF on redox state markers in different tissues in order to uncover how changes in feeding frequency alter redox balance in rats. IF rats displayed lower body mass due to decreased energy conversion efficiency. Livers in IF rats presented increased mitochondrial respiratory capacity and enhanced levels of protein carbonyls. Surprisingly, IF animals also presented an increase in oxidative damage in the brain that was not related to changes in mitochondrial bioenergetics. Conversely, IF promoted a substantial protection against oxidative damage in the heart. No difference in mitochondrial bioenergetics or redox homeostasis was observed in skeletal muscles of IF animals. Overall, IF affects redox balance in a tissue-specific manner, leading to redox imbalance in the liver and brain and protection against oxidative damage in the heart. 相似文献
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叶黄素酯对四氧嘧啶所致小鼠氧化损伤的保护性研究 总被引:1,自引:0,他引:1
目的研究万寿菊花中提取的叶黄素酯体内对四氧嘧啶所致的小鼠氧化损伤的影响。方法采用分光光度法测定模型组肝组织超氧化物歧化酶(SOD)、丙二醛(MDA)、过氧化氢酶(CAT)、谷脱甘肽(GSH)、血清中天门冬氨酶氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)、肝糖原,脑、心脏、股四头肌SOD、MDA的活性。结果叶黄素酯可抑制由于氧化损伤所致的小鼠肝SOD、MDA、CAT、GSH和血清中AST、AIJT的异常升高;降低脑、心脏、股四头肌SOD、MDA水平;降低血糖,提高肝糖元水平。结论叶黄素可通过影响组织、血清中相关酶活性而对四氧嘧啶所致的小鼠氧化损伤有一定的保护作用。 相似文献
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Kwong LK Kamzalov S Rebrin I Bayne AC Jana CK Morris P Forster MJ Sohal RS 《Free radical biology & medicine》2002,33(5):627-638
Coenzyme Q (CoQ(10)) is a component of the mitochondrial electron transport chain and also a constituent of various cellular membranes. It acts as an important in vivo antioxidant, but is also a primary source of O(2)(-*)/H(2)O(2) generation in cells. CoQ has been widely advocated to be a beneficial dietary adjuvant. However, it remains controversial whether oral administration of CoQ can significantly enhance its tissue levels and/or can modulate the level of oxidative stress in vivo. The objective of this study was to determine the effect of dietary CoQ supplementation on its content in various tissues and their mitochondria, and the resultant effect on the in vivo level of oxidative stress. Rats were administered CoQ(10) (150 mg/kg/d) in their diets for 4 and 13 weeks; thereafter, the amounts of CoQ(10) and CoQ(9) were determined by HPLC in the plasma, homogenates of the liver, kidney, heart, skeletal muscle, brain, and mitochondria of these tissues. Administration of CoQ(10) increased plasma and mitochondria levels of CoQ(10) as well as its predominant homologue CoQ(9). Generally, the magnitude of the increases was greater after 13 weeks than 4 weeks. The level of antioxidative defense enzymes in liver and skeletal muscle homogenates and the rate of hydrogen peroxide generation in heart, brain, and skeletal muscle mitochondria were not affected by CoQ supplementation. However, a reductive shift in plasma aminothiol status and a decrease in skeletal muscle mitochondrial protein carbonyls were apparent after 13 weeks of supplementation. Thus, CoQ supplementation resulted in an elevation of CoQ homologues in tissues and their mitochondria, a selective decrease in protein oxidative damage, and an increase in antioxidative potential in the rat. 相似文献