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Carbonyl Levels (carbonyl + level)
Selected AbstractsBeneficial effects of aminoguanidine on the cardiovascular system of diabetic ratsDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2005Krisztián Stadler Abstract Background The study focused on investigating the effect of aminoguanidine on cardiovascular damages in diabetes and the possible mechanisms of its action. Methods Aminoguanidine (AMNG) was used to treat streptozotocin-induced diabetic rats, and the effects were compared to those obtained under insulin treatment. Blood metabolic parameters, ,NO and ONOO, as well as protein carbonyl levels and cardiac hypertrophy were determined. Results Diabetic animals showed increased ,NO levels and markedly increased ONOO, generation in the aorta, along with a significant hypertrophy and protein carbonylation in the cardiac tissue. Both AMNG and insulin treatment suppressed the levels of overproduced ,NO or ONOO, in the vasculature, but only AMNG was able to prevent hypertrophic alterations and reduce protein carbonylation in the cardiac tissue. Conclusions Oxidative protein modification, together with cardiac hypertrophy and high generation of ,NO and ONOO,, are important early events in the development of cardiovascular complications in diabetes. Aminoguanidine could prevent hypertrophy through inhibition of production of nonenzymatic glycation products rather than via inhibition of ,NO production. Copyright © 2004 John Wiley & Sons, Ltd. [source] Detection of carbonyl-modified proteins in interfibrillar rat mitochondria using N, -aminooxymethylcarbonylhydrazino- D -biotin as an aldehyde/keto-reactive probe in combination with Western blot analysis and tandem mass spectrometryELECTROPHORESIS, Issue 6 2008Woon-Gye Chung Abstract There is now a large body of supporting data available that links oxidative modifications of proteins to a large number of diseases, degenerative disorders and aging. However, the detailed analysis of oxidative protein modifications remains challenging. Here, we report a new efficient method for identification of oxidatively modified proteins in complex biological samples which is based on the use of an aldehyde-reactive probe, N,-aminooxymethylcarbonylhydrazino- D -biotin (ARP), in combination with Western-type analyses and MS. The biotinylated hydroxylamine derivative forms a chemically stable oxime derivative with the aldehyde/keto group found in carbonyl-modified proteins. The biotin tag is detected by avidin affinity staining. ARP-positive proteins are subsequently subjected to in-gel trypsinization and MS/MS for protein identification. We demonstrate the usefulness of the method for the analysis of protein extracts obtained from interfibrillar heart mitochondria (IFM) from young and old rats. In this study, we identified as putative major protein targets of oxidative modifications the mitochondrial matrix protein, aconitase, the inner mitochondrial membrane protein, ADP/ATP translocase, and constituents of the electron transport chain complexes IV and V. An age-related increase of carbonyl levels was found for aconitase and ATP synthase. [source] Melatonin protects against taurolithocholic-induced oxidative stress in rat liverJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 5 2010Lorena Fuentes-Broto Abstract Cholestasis, encountered in a variety of clinical disorders, is characterized by intracellular accumulation of toxic bile acids in the liver. Furthermore, oxidative stress plays an important role in the pathogenesis of bile acids. Taurolithocholic acid (TLC) was revealed in previous studies as the most pro-oxidative bile acid. Melatonin, a well-known antioxidant, is a safe and widely used therapeutic agent. Herein, we investigated the hepatoprotective role of melatonin on lipid and protein oxidation induced by TLC alone and in combination with FeCl3 and ascorbic acid in rat liver homogenates and hepatic membranes. The lipid peroxidation products, malondialdehyde and 4-hydroxyalkenals (MDA,+,4-HDA), and carbonyl levels were quantified as indices of oxidative damage to hepatic lipids and proteins, respectively. In the current study, the rise in MDA,+,4-HDA levels induced by TLC was inhibited by melatonin in a concentration-dependent manner in both liver homogenates and in hepatic membranes. Melatonin also had protective effects against structural damage to proteins induced by TLC in membranes. These results suggest that the indoleamine melatonin may potentially act as a protective agent in the therapy of those diseases that involve bile acid toxicity. J. Cell. Biochem. 110: 1219,1225, 2010. Published 2010 Wiley-Liss, Inc. [source] Differential effects of the mitochondrial uncoupling agent, 2,4-dinitrophenol, or the nitroxide antioxidant, Tempol, on synaptic or nonsynaptic mitochondria after spinal cord injuryJOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2009Samir P. Patel Abstract We recently documented the progressive nature of mitochondrial dysfunction over 24 hr after contusion spinal cord injury (SCI), but the underlying mechanism has not been elucidated. We investigated the effects of targeting two distinct possible mechanisms of mitochondrial dysfunction by using the mitochondrial uncoupler 2,4-dinitrophenol (2,4-DNP) or the nitroxide antioxidant Tempol after contusion SCI in rats. A novel aspect of this study was that all assessments were made in both synaptosomal (neuronal)- and nonsynaptosomal (glial and neuronal soma)-derived mitochondria 24 hr after injury. Mitochondrial uncouplers target Ca2+ cycling and subsequent reactive oxygen species production in mitochondria after injury. When 2,4-DNP was injected 15 and 30 min after injury, mitochondrial function was preserved in both populations compared with vehicle-treated rats, whereas 1 hr postinjury treatment was ineffective. Conversely, targeting peroxynitrite with Tempol failed to maintain normal bioenergetics in synaptic mitochondria, but was effective in nonsynaptic mitochondria when administered 15 min after injury. When administered at 15 and 30 min after injury, increased hydroxynonenal, 3-NT, and protein carbonyl levels were significantly reduced by 2,4-DNP, whereas Tempol only reduced 3-NT and protein carbonyls after SCI. Despite such antioxidant effects, only 2,4-DNP was effective in preventing mitochondrial dysfunction, indicating that mitochondrial Ca2+ overload may be the key mechanism involved in acute mitochondrial damage after SCI. Collectively, our observations demonstrate the significant role that mitochondrial dysfunction plays in SCI neuropathology. Moreover, they indicate that combinatorial therapeutic approaches targeting different populations of mitochondria holds great potential in fostering neuroprotection after acute SCI. © 2008 Wiley-Liss, Inc. [source] Difluoromethylornithine Decreases Long-Lasting Protein Oxidation Induced by Neonatal Ethanol Exposure in the Hippocampus of Adolescent RatsALCOHOLISM, Issue 5 2007Carlos Fernando Mello Background: Ethanol exposure and withdrawal during central nervous system development can cause oxidative stress and produce severe and long-lasting behavioral and morphological alterations in which polyamines seem to play an important role. However, it is not known if early ethanol exposure causes long-lasting protein oxidative damage and if polyamines play a role in such a deleterious effect of ethanol. Methods: In this study we investigated the effects of early ethanol exposure (6 g/kg/d, by gavage), from postnatal day (PND) 1 to 8, and of the administration of difluoromethylornithine (DFMO, 500 mg/kg, i.p., on PND 8), a polyamine biosynthesis inhibitor, on the extent of oxidative modification of proteins. Indices of oxidative modification of proteins included protein carbonyls, 3-nitrotyrosine (3-NT), and protein bound 4-hydroxynonenal (HNE) in the hippocampus, cerebellum, hypothalamus, striatum, and cerebral cortex of Sprague,Dawley rats at PND 40. Results: Both ethanol and DFMO administration alone increased protein carbonyl immunoreactivity in the hippocampus at PND 40, but the combination of DFMO and ethanol resulted in no effect on protein carbonyl levels. No alterations in the content of protein-bound HNE, 3-NT, or carbonyl were found in any other cerebral structure. Conclusions: These results suggest that the hippocampus is selectively affected by early ethanol exposure and by polyamine synthesis inhibition. In addition, the results suggest a role for polyamines in the long-lasting increase of protein carbonyls induced by ethanol exposure and withdrawal. [source] Distinct physiological responses of two rice cultivars subjected to iron toxicity under field conditionsANNALS OF APPLIED BIOLOGY, Issue 2 2009R.J. Stein Abstract Iron toxicity is recognised as the most widely distributed nutritional disorder in lowland and irrigated rice, derived from the excessive amounts of ferrous ions generated by the reduction of iron oxides in flooded soils. Rice cultivars with variable degrees of tolerance to iron toxicity have been developed, and cultural practices such as water management and fertilisation can be used to reduce its negative impact. However, because of the complex nature of iron toxicity, few physiological data concerning tolerance mechanisms to excess iron in field conditions are available. To analyse the physiological responses of rice to iron excess in field conditions, two rice cultivars with distinct tolerance to iron toxicity [BR-IRGA 409 (susceptible) and IRGA 420 (tolerant)] were grown in two areas, with a well-established history of iron toxicity (in Camaquã, RS, Brazil) and without iron toxicity (in Cachoeirinha, RS, Brazil). Plants from the susceptible cultivar grown in the iron-toxic site showed lower levels of chlorophylls and soluble proteins (together with higher carbonyl levels) indicating photooxidative and oxidative damage. The toxic effects observed were because of the accumulation of high levels of iron and not because of any indirectly induced shoot deficiency of other nutrients. Higher activities of antioxidative enzymes were also observed in leaves of plants from the susceptible cultivar only in the iron-toxic site, probably as a result of oxidative stress rather than because of specific involvement in a tolerance mechanism. There was no difference between cultivars in iron accumulation in the symplastic and apoplastic space of leaves, with both cultivars accumulating 85,90% of total leaf iron in the symplast. However, susceptible plants accumulated higher levels of iron in low-molecular-mass fractions than tolerant plants. The accumulation of iron in the low-molecular-mass fraction probably has a direct influence on iron toxicity, and the adaptive strategy of tolerant plants may rely on their capacity to buffer the iron amounts present in the low mass fraction, a new parameter to be considered when evaluating tolerance to iron excess in field-cultivated rice plants. [source] Relationship between oxidative stress-related biomarkers and antioxidant status with asthma and atopy in young adults: a population-based studyCLINICAL & EXPERIMENTAL ALLERGY, Issue 3 2009V. García-Larsen Summary Background and aim Enhanced oxidative stress has been described in adults who suffer from symptoms of asthma and poor lung function. This study assessed the relation between markers of oxidative stress and antioxidant status and lung function, symptoms of asthma, atopy and bronchial hyperresponsiveness (BHR) in young adults. Methods A sub-sample of 589 individuals aged 22,28 years, selected from a total of 1232 included in a survey assessing early and current risk factors for chronic diseases, participated in the study. Participants were from an agricultural area of Chile, responded to a Spanish version of the European Community Respiratory Health Survey questionnaire, were skin tested to eight allergens, and challenged with methacholine to assess BHR. Five hundred and eighty-five individuals had measures of plasma biomarkers ferric reducing ability of plasma, uric acid, protein carbonyls and 564 had 8-iso-prostaglandin F2, (8-iso-PGF2,) assessed. Results All participants had detectable plasma 8-iso-PGF2, and carbonyl levels. There was no indication for an association between markers of antioxidant status or oxidative stress with any of the outcomes studied. Conclusion The levels of oxidative stress-related biomarkers and antioxidant status in plasma may not be related to asthma in the general population in the absence of more severe symptoms or exacerbations. [source] Effects of melatonin on the oxidant/antioxidant status and lung histopathology in rabbits exposed to cigarette smokeRESPIROLOGY, Issue 4 2006Mehmet UNLU Objectives and background: To evaluate the effects of cigarette smoking on the histopathology and the oxidant/antioxidant status of the lungs and to test the potential antioxidant benefits of melatonin on these induced changes. Methodology: Rabbits were exposed to cigarette smoke in a glass chamber for 1 h daily for 1 month with or without intraperitoneal melatonin injection. A melatonin control group was given intraperitoneal melatonin only. A control group was exposed to clean air only. At the end of 1 month, animals were sacrificed and lung tissues were examined histopathologically. Blood levels of protein sulphydryls, carbonyls, prostaglandin F2, (PGF2,), malondialdehyde (MDA), glutathione peroxidase and superoxide dismutase (SOD) were measured. Results: Intraparenchymal vascular congestion and thrombosis, intraparenchymal haemorrhage, respiratory epithelial proliferation, number of macrophages in the alveolar and bronchial lumen, alveolar destruction, emphysematous changes and bronchoalveolar haemorrhage scores were significantly increased in rabbits exposed to cigarette smoke compared with the control group. Protein sulphydryls and SOD levels were significantly decreased; carbonyls, PGF2, and MDA levels were significantly increased in the smoke exposed rabbits. Administration of melatonin to rabbits exposed to cigarette smoke caused a reduction in the bronchoalveolar haemorrhage score and blood carbonyls levels. Other parameters were unaffected by melatonin. Conclusion: Exposure to cigarette smoke causes severe histopathological changes and negatively affects the oxidant/antioxidant status in the lungs of rabbits. A low daily dose of melatonin has some protective effects on histopathological changes and oxidant/antioxidant status of the lungs in smoke exposed rabbits. [source] | |||||||||||||