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Jurandir Fernando Comar - One of the best experts on this subject based on the ideXlab platform.
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Oxidative state and oxidative metabolism of the heart from rats with Adjuvant-Induced Arthritis.
Experimental and molecular pathology, 2016Co-Authors: Amanda Caroline Schubert, Mariana Marques Nogueira Wendt, Anacharis Babeto De Sá-nakanishi, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Jurandir Fernando Comar, Adelar BrachtAbstract:The aim of the present work was to investigate, in a more extensive way, the oxidative state and parameters related to energy metabolism of the heart tissue of rats using the model of Adjuvant-Induced Arthritis. The latter is a model for the human arthritic disease. Measurements were done in the total tissue homogenate, isolated mitochondria and cytosolic fraction. The Adjuvant-Induced Arthritis caused several modifications in the oxidative state of the heart which, in general, indicate an increased oxidative stress (+80% reactive oxygen species), protein damage (+53% protein carbonyls) and lipid damage (+63% peroxidation) in the whole tissue. The distribution of these changes over the various cell compartments was frequently unequal. For example, protein carbonyls were increased in the whole tissue and in the cytosol, but not in the mitochondria. No changes in GSH content of the whole tissue were found, but it was increased in the mitochondria (+33%) and decreased in the cytosol (-19%). The activity of succinate dehydrogenase was 77% stimulated by Arthritis; the activities of glutamate dehydrogenase, isocitrate dehydrogenase and cytochrome c oxidase were diminished by 31, 25 and 35.3%, respectively. In spite of these alterations, no changes in the mitochondrial respiratory activity and in the efficiency of energy transduction were found. It can be concluded that the Adjuvant-Induced Arthritis in rats causes oxidative damage to the heart with an unequal intracellular distribution. Compared to the liver and brain the modifications caused by Arthritis in the heart are less pronounced on variables such as GSH levels and protein integrity. Possibly this occurs because the antioxidant system of the heart is less impaired by Arthritis than that reported for the former tissues. Even so, the modifications caused by Arthritis represent an imbalanced situation that probably contributes to the cardiac symptoms of the Arthritis disease.
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Oxidative state and oxidative metabolism in the brain of rats with Adjuvant-Induced Arthritis.
Experimental and Molecular Pathology, 2015Co-Authors: Mariana Marques Nogueira Wendt, Anacharis Babeto De Sá-nakanishi, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Adelar Bracht, Cristiane Vizioli De Castro Ghizoni, Jurandir Fernando ComarAbstract:The aim of the present work was to investigate, in a more extensive way, the oxidative state and parameters related to energy metabolism of the heart tissue of rats using the model of Adjuvant-Induced Arthritis. The latter is a model for the human arthritic disease. Measurements were done in the total tissue homogenate, isolated mitochondria and cytosolic fraction. The Adjuvant-Induced Arthritis caused several modifications in the oxidative state of the heart which, in general, indicate an increased oxidative stress (+80% reactive oxygen species), protein damage (+53% protein carbonyls) and lipid damage (+63% peroxidation) in the whole tissue. The distribution of these changes over the various cell compartments was frequently unequal. For example, protein carbonyls were increased in the whole tissue and in the cytosol, but not in the mitochondria. No changes in GSH content of the whole tissue were found, but it was increased in the mitochondria (+33%) and decreased in the cytosol (-19%). The activity of succinate dehydrogenase was 77% stimulated by Arthritis; the activities of glutamate dehydrogenase, isocitrate dehydrogenase and cytochrome c oxidase were diminished by 31, 25 and 35.3%, respectively. In spite of these alterations, no changes in the mitochondrial respiratory activity and in the efficiency of energy transduction were found. It can be concluded that the Adjuvant-Induced Arthritis in rats causes oxidative damage to the heart with an unequal intracellular distribution. Compared to the liver and brain the modifications caused by Arthritis in the heart are less pronounced on variables such as GSH levels and protein integrity. Possibly this occurs because the antioxidant system of the heart is less impaired by Arthritis than that reported for the former tissues. Even so, the modifications caused by Arthritis represent an imbalanced situation that probably contributes to the cardiac symptoms of the Arthritis disease.
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Oxidative state and oxidative metabolism in the brain of rats with Adjuvant-Induced Arthritis.
Experimental and molecular pathology, 2015Co-Authors: Mariana Marques Nogueira Wendt, Anacharis Babeto De Sá-nakanishi, Rosane Marina Peralta, Adelar Bracht, Cristiane Vizioli De Castro Ghizoni, Ciomar Aparecida Bersani Amado, Jurandir Fernando ComarAbstract:The purpose of the present study was to evaluate the oxidative status of the brain of arthritic rats, based mainly on the observation that Arthritis induces a pronounced oxidative stress in the liver of Arthritis rats and that morphological alterations have been reported to occur in patients with rheumatoid Arthritis. Rats with Adjuvant-Induced Arthritis were used. These animals presented higher levels of reactive oxygen species (ROS) in the total brain homogenate (25% higher) and in the mitochondria (+55%) when compared to healthy rats. The nitrite plus nitrate contents, nitric oxide (NO) markers, were also increased in both mitochondria (+27%) and cytosol (+14%). Arthritic rats also presented higher levels of protein carbonyl groups in the total homogenate (+43%), mitochondria (+69%) and cytosol (+145%). Arthritis caused a diminution of oxygen consumption in isolated brain mitochondria only when ascorbate was the electron donor. The disease diminished the mitochondrial cytochrome c oxidase activity by 55%, but increased the transmembrane potential by 16%. The pro-oxidant enzyme xanthine oxidase was 150%, 110% and 283% higher, respectively, in the brain homogenate, mitochondria and cytosol of arthritic animals. The same occurred with the calcium-independent NO-synthase activity that was higher in the brain homogenate (90%) and cytosol (122%) of arthritic rats. The catalase activity, on the other hand, was diminished by Arthritis in all cellular fractions (between 30 and 40%). It is apparent that the brain of rats with Adjuvant-Induced Arthritis presents a pronounced oxidative stress and a significant injury to lipids and proteins, a situation that possibly contributes to the brain symptoms of the Arthritis disease.
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oxidative state of the liver of rats with adjuvant induced Arthritis
Free Radical Biology and Medicine, 2013Co-Authors: Jurandir Fernando Comar, Mariana Marques Nogueira Wendt, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Anacharis Babeto De Sanakanishi, Andrea Luiza De Oliveira, Emy Luiza Ishii Iwamoto, Adelar BrachtAbstract:Adjuvant-Induced Arthritis is an experimental immunopathology in rats that is often used as a model for studying autoimmune chronic inflammation and inflammatory cachexia. In these animals oxidative stress is quite pronounced in the articular inflammation sites. The purpose of this study was to evaluate oxidative stress in the liver of arthritic rats in which morphological and metabolic alterations have been reported to occur. Oxidative injury parameters, levels and production of reactive oxygen species (ROS), and antioxidant parameters were measured in the total liver homogenate and in subcellular fractions, namely cytosol, mitochondria, and peroxisomes. Arthritic rats presented higher levels of ROS than controls in the total homogenate (46% higher) and in all subcellular fractions (51, 38, and 55% higher for mitochondria, peroxisome, and cytosol, respectively). Arthritic rats also presented higher levels of protein carbonyl groups in the total homogenate (75%) and in all subcellular fractions (189, 227, and 260%, respectively, for mitochondria, peroxisomes, and cytosol). The TBARS levels of arthritic rats were more elevated in the total homogenate (36%), mitochondria (20%), and peroxisomes (16%). Arthritic rats also presented higher levels of NO markers in the peroxisomes (112%) and in the cytosol (35%). The catalase activity of all cell compartments was strongly diminished (between 77 and 87%) by Arthritis, and glutathione peroxidase activities were diminished in the mitochondria (33.7%) and cytosol (41%). The cytosolic glucose-6-phosphate dehydrogenase activity, on the other hand, was increased (62.9%), the same happening with inducible peroxisomal NO synthase (119.3%). The superoxide dismutase and glutathione reductase activities were not affected. The GSH content was diminished by Arthritis in all cellular compartments (50 to 59% diminution). The results reveal that the liver of rats with Adjuvant-Induced Arthritis presents a pronounced oxidative stress and that, in consequence, injury to lipids and proteins is highly significant. The higher ROS content of the liver of arthritic rats seems to be the consequence of both a stimulated pro-oxidant system and a deficient antioxidant defense with a predominance of the latter as indicated by the strongly diminished activities of catalase and glutathione peroxidase.
Adelar Bracht - One of the best experts on this subject based on the ideXlab platform.
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Oxidative state and oxidative metabolism of the heart from rats with Adjuvant-Induced Arthritis.
Experimental and molecular pathology, 2016Co-Authors: Amanda Caroline Schubert, Mariana Marques Nogueira Wendt, Anacharis Babeto De Sá-nakanishi, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Jurandir Fernando Comar, Adelar BrachtAbstract:The aim of the present work was to investigate, in a more extensive way, the oxidative state and parameters related to energy metabolism of the heart tissue of rats using the model of Adjuvant-Induced Arthritis. The latter is a model for the human arthritic disease. Measurements were done in the total tissue homogenate, isolated mitochondria and cytosolic fraction. The Adjuvant-Induced Arthritis caused several modifications in the oxidative state of the heart which, in general, indicate an increased oxidative stress (+80% reactive oxygen species), protein damage (+53% protein carbonyls) and lipid damage (+63% peroxidation) in the whole tissue. The distribution of these changes over the various cell compartments was frequently unequal. For example, protein carbonyls were increased in the whole tissue and in the cytosol, but not in the mitochondria. No changes in GSH content of the whole tissue were found, but it was increased in the mitochondria (+33%) and decreased in the cytosol (-19%). The activity of succinate dehydrogenase was 77% stimulated by Arthritis; the activities of glutamate dehydrogenase, isocitrate dehydrogenase and cytochrome c oxidase were diminished by 31, 25 and 35.3%, respectively. In spite of these alterations, no changes in the mitochondrial respiratory activity and in the efficiency of energy transduction were found. It can be concluded that the Adjuvant-Induced Arthritis in rats causes oxidative damage to the heart with an unequal intracellular distribution. Compared to the liver and brain the modifications caused by Arthritis in the heart are less pronounced on variables such as GSH levels and protein integrity. Possibly this occurs because the antioxidant system of the heart is less impaired by Arthritis than that reported for the former tissues. Even so, the modifications caused by Arthritis represent an imbalanced situation that probably contributes to the cardiac symptoms of the Arthritis disease.
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Oxidative state and oxidative metabolism in the brain of rats with Adjuvant-Induced Arthritis.
Experimental and Molecular Pathology, 2015Co-Authors: Mariana Marques Nogueira Wendt, Anacharis Babeto De Sá-nakanishi, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Adelar Bracht, Cristiane Vizioli De Castro Ghizoni, Jurandir Fernando ComarAbstract:The aim of the present work was to investigate, in a more extensive way, the oxidative state and parameters related to energy metabolism of the heart tissue of rats using the model of Adjuvant-Induced Arthritis. The latter is a model for the human arthritic disease. Measurements were done in the total tissue homogenate, isolated mitochondria and cytosolic fraction. The Adjuvant-Induced Arthritis caused several modifications in the oxidative state of the heart which, in general, indicate an increased oxidative stress (+80% reactive oxygen species), protein damage (+53% protein carbonyls) and lipid damage (+63% peroxidation) in the whole tissue. The distribution of these changes over the various cell compartments was frequently unequal. For example, protein carbonyls were increased in the whole tissue and in the cytosol, but not in the mitochondria. No changes in GSH content of the whole tissue were found, but it was increased in the mitochondria (+33%) and decreased in the cytosol (-19%). The activity of succinate dehydrogenase was 77% stimulated by Arthritis; the activities of glutamate dehydrogenase, isocitrate dehydrogenase and cytochrome c oxidase were diminished by 31, 25 and 35.3%, respectively. In spite of these alterations, no changes in the mitochondrial respiratory activity and in the efficiency of energy transduction were found. It can be concluded that the Adjuvant-Induced Arthritis in rats causes oxidative damage to the heart with an unequal intracellular distribution. Compared to the liver and brain the modifications caused by Arthritis in the heart are less pronounced on variables such as GSH levels and protein integrity. Possibly this occurs because the antioxidant system of the heart is less impaired by Arthritis than that reported for the former tissues. Even so, the modifications caused by Arthritis represent an imbalanced situation that probably contributes to the cardiac symptoms of the Arthritis disease.
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Oxidative state and oxidative metabolism in the brain of rats with Adjuvant-Induced Arthritis.
Experimental and molecular pathology, 2015Co-Authors: Mariana Marques Nogueira Wendt, Anacharis Babeto De Sá-nakanishi, Rosane Marina Peralta, Adelar Bracht, Cristiane Vizioli De Castro Ghizoni, Ciomar Aparecida Bersani Amado, Jurandir Fernando ComarAbstract:The purpose of the present study was to evaluate the oxidative status of the brain of arthritic rats, based mainly on the observation that Arthritis induces a pronounced oxidative stress in the liver of Arthritis rats and that morphological alterations have been reported to occur in patients with rheumatoid Arthritis. Rats with Adjuvant-Induced Arthritis were used. These animals presented higher levels of reactive oxygen species (ROS) in the total brain homogenate (25% higher) and in the mitochondria (+55%) when compared to healthy rats. The nitrite plus nitrate contents, nitric oxide (NO) markers, were also increased in both mitochondria (+27%) and cytosol (+14%). Arthritic rats also presented higher levels of protein carbonyl groups in the total homogenate (+43%), mitochondria (+69%) and cytosol (+145%). Arthritis caused a diminution of oxygen consumption in isolated brain mitochondria only when ascorbate was the electron donor. The disease diminished the mitochondrial cytochrome c oxidase activity by 55%, but increased the transmembrane potential by 16%. The pro-oxidant enzyme xanthine oxidase was 150%, 110% and 283% higher, respectively, in the brain homogenate, mitochondria and cytosol of arthritic animals. The same occurred with the calcium-independent NO-synthase activity that was higher in the brain homogenate (90%) and cytosol (122%) of arthritic rats. The catalase activity, on the other hand, was diminished by Arthritis in all cellular fractions (between 30 and 40%). It is apparent that the brain of rats with Adjuvant-Induced Arthritis presents a pronounced oxidative stress and a significant injury to lipids and proteins, a situation that possibly contributes to the brain symptoms of the Arthritis disease.
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oxidative state of the liver of rats with adjuvant induced Arthritis
Free Radical Biology and Medicine, 2013Co-Authors: Jurandir Fernando Comar, Mariana Marques Nogueira Wendt, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Anacharis Babeto De Sanakanishi, Andrea Luiza De Oliveira, Emy Luiza Ishii Iwamoto, Adelar BrachtAbstract:Adjuvant-Induced Arthritis is an experimental immunopathology in rats that is often used as a model for studying autoimmune chronic inflammation and inflammatory cachexia. In these animals oxidative stress is quite pronounced in the articular inflammation sites. The purpose of this study was to evaluate oxidative stress in the liver of arthritic rats in which morphological and metabolic alterations have been reported to occur. Oxidative injury parameters, levels and production of reactive oxygen species (ROS), and antioxidant parameters were measured in the total liver homogenate and in subcellular fractions, namely cytosol, mitochondria, and peroxisomes. Arthritic rats presented higher levels of ROS than controls in the total homogenate (46% higher) and in all subcellular fractions (51, 38, and 55% higher for mitochondria, peroxisome, and cytosol, respectively). Arthritic rats also presented higher levels of protein carbonyl groups in the total homogenate (75%) and in all subcellular fractions (189, 227, and 260%, respectively, for mitochondria, peroxisomes, and cytosol). The TBARS levels of arthritic rats were more elevated in the total homogenate (36%), mitochondria (20%), and peroxisomes (16%). Arthritic rats also presented higher levels of NO markers in the peroxisomes (112%) and in the cytosol (35%). The catalase activity of all cell compartments was strongly diminished (between 77 and 87%) by Arthritis, and glutathione peroxidase activities were diminished in the mitochondria (33.7%) and cytosol (41%). The cytosolic glucose-6-phosphate dehydrogenase activity, on the other hand, was increased (62.9%), the same happening with inducible peroxisomal NO synthase (119.3%). The superoxide dismutase and glutathione reductase activities were not affected. The GSH content was diminished by Arthritis in all cellular compartments (50 to 59% diminution). The results reveal that the liver of rats with Adjuvant-Induced Arthritis presents a pronounced oxidative stress and that, in consequence, injury to lipids and proteins is highly significant. The higher ROS content of the liver of arthritic rats seems to be the consequence of both a stimulated pro-oxidant system and a deficient antioxidant defense with a predominance of the latter as indicated by the strongly diminished activities of catalase and glutathione peroxidase.
Andrew H. Kang - One of the best experts on this subject based on the ideXlab platform.
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Adjuvant-Induced Arthritis in rats. Evidence that autoimmunity to homologous collagens types I, II, IX and XI is not involved in the pathogenesis of Arthritis.
Clinical and experimental immunology, 2008Co-Authors: M. A. Cremer, A. S. Townes, Andrew H. KangAbstract:We examined the sera of arthritic outbred Wistar and Sprague-Dawley rats and inbred Fisher 344 and Wistar-Lewis rats for autoantibodies to rat type I, II, IX and XI collagens following the induction of Arthritis with mycobacteria (MTB). Although many sera collected over an extended time were assayed in addition to acid eluates of arthritic joints, convincing evidence for autoimmunity to collagen could not be demonstrated. Instead, modest non-specific reactions were observed to collagen, irrelevant proteins, and buffer-treated plastic microtitre wells. In contrast, antibodies to purified protein derivative (PPD) were detected in the sera of rats developing Adjuvant-Induced Arthritis, and antibodies to type II collagen, in the sera and joint eluate of rats developing experimental collagen-induced Arthritis. Lastly, delayed-type hypersensitivity responses to collagen could not be detected, nor could Adjuvant-Induced Arthritis be attenuated by soluble collagen injected intravenously before challenge with MTB. We conclude that Adjuvant-Induced Arthritis and experimental collagen-induced Arthritis are distinct models of rheumatic disease and that autoimmunity to collagen is neither prevalent in Adjuvant-Induced Arthritis nor necessary for its pathogenesis.
Jeanmarie Besson - One of the best experts on this subject based on the ideXlab platform.
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c fos expression in rat lumbar spinal cord during the development of adjuvant induced Arthritis
Neuroscience, 1992Co-Authors: C Abbadie, Jeanmarie BessonAbstract:Abstract A parallel clinical and behavioral study of Adjuvant-Induced Arthritis in the rat showed four stages in the time-course of the disease: preclinical (first week), acute (weeks 2–4), post-acute (weeks 5–8) and recovery weeks 9–11) [Calvino et al. (1987) Behav. Brain Res.24, 11–29]. As several studies have reported the expression of the proto-oncogene c-fos in spinal cord neurons following acute noxious peripheral stimuli, the aim of this study was to quantitatively assess Fos-like immunoreactivity in lumbar spinal cord neurons at various times of Adjuvant-Induced Arthritis development, i.e. one, two, three, 11 and 22 weeks post-inoculation. The total number of Fos-like immunoreactive neurons in the lumbar enlargement correlated with the observed development of Adjuvant-Induced Arthritis, i.e. Fos-like immunoreactivity was absent at one week, moderate at two weeks, greatly increased at three weeks, decreased at 11 weeks and returned to control values at 22 weeks. At three weeks, at the peak of Fos-like immunoreactivity distribution and acute stage of hyperalgesia, maximal labeling was observed in L3 and L4 spinal segments. In these segments, the most densely labeled region was the neck (laminae V and VI) of the dorsal horn (55%) and the ventral horn (35%) as compared to the superficial laminae (laminae I and II; 5%) and the nucleus proprius (laminae III and IV; 5%). These data indicate that c-fos expression induced by chronic inflammation is better expressed in deeper laminae than in the superficial ones, and that the number of Fos-positive cells correlates with behavioral studies. Thus, the use of Fos-like immunoreactivity in the chronic inflammatory pain model seems to be an interesting tool to study possible effects of various pharmacological compounds such as analgesic or anti-inflammatory drugs.
Mariana Marques Nogueira Wendt - One of the best experts on this subject based on the ideXlab platform.
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Oxidative state and oxidative metabolism of the heart from rats with Adjuvant-Induced Arthritis.
Experimental and molecular pathology, 2016Co-Authors: Amanda Caroline Schubert, Mariana Marques Nogueira Wendt, Anacharis Babeto De Sá-nakanishi, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Jurandir Fernando Comar, Adelar BrachtAbstract:The aim of the present work was to investigate, in a more extensive way, the oxidative state and parameters related to energy metabolism of the heart tissue of rats using the model of Adjuvant-Induced Arthritis. The latter is a model for the human arthritic disease. Measurements were done in the total tissue homogenate, isolated mitochondria and cytosolic fraction. The Adjuvant-Induced Arthritis caused several modifications in the oxidative state of the heart which, in general, indicate an increased oxidative stress (+80% reactive oxygen species), protein damage (+53% protein carbonyls) and lipid damage (+63% peroxidation) in the whole tissue. The distribution of these changes over the various cell compartments was frequently unequal. For example, protein carbonyls were increased in the whole tissue and in the cytosol, but not in the mitochondria. No changes in GSH content of the whole tissue were found, but it was increased in the mitochondria (+33%) and decreased in the cytosol (-19%). The activity of succinate dehydrogenase was 77% stimulated by Arthritis; the activities of glutamate dehydrogenase, isocitrate dehydrogenase and cytochrome c oxidase were diminished by 31, 25 and 35.3%, respectively. In spite of these alterations, no changes in the mitochondrial respiratory activity and in the efficiency of energy transduction were found. It can be concluded that the Adjuvant-Induced Arthritis in rats causes oxidative damage to the heart with an unequal intracellular distribution. Compared to the liver and brain the modifications caused by Arthritis in the heart are less pronounced on variables such as GSH levels and protein integrity. Possibly this occurs because the antioxidant system of the heart is less impaired by Arthritis than that reported for the former tissues. Even so, the modifications caused by Arthritis represent an imbalanced situation that probably contributes to the cardiac symptoms of the Arthritis disease.
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Oxidative state and oxidative metabolism in the brain of rats with Adjuvant-Induced Arthritis.
Experimental and Molecular Pathology, 2015Co-Authors: Mariana Marques Nogueira Wendt, Anacharis Babeto De Sá-nakanishi, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Adelar Bracht, Cristiane Vizioli De Castro Ghizoni, Jurandir Fernando ComarAbstract:The aim of the present work was to investigate, in a more extensive way, the oxidative state and parameters related to energy metabolism of the heart tissue of rats using the model of Adjuvant-Induced Arthritis. The latter is a model for the human arthritic disease. Measurements were done in the total tissue homogenate, isolated mitochondria and cytosolic fraction. The Adjuvant-Induced Arthritis caused several modifications in the oxidative state of the heart which, in general, indicate an increased oxidative stress (+80% reactive oxygen species), protein damage (+53% protein carbonyls) and lipid damage (+63% peroxidation) in the whole tissue. The distribution of these changes over the various cell compartments was frequently unequal. For example, protein carbonyls were increased in the whole tissue and in the cytosol, but not in the mitochondria. No changes in GSH content of the whole tissue were found, but it was increased in the mitochondria (+33%) and decreased in the cytosol (-19%). The activity of succinate dehydrogenase was 77% stimulated by Arthritis; the activities of glutamate dehydrogenase, isocitrate dehydrogenase and cytochrome c oxidase were diminished by 31, 25 and 35.3%, respectively. In spite of these alterations, no changes in the mitochondrial respiratory activity and in the efficiency of energy transduction were found. It can be concluded that the Adjuvant-Induced Arthritis in rats causes oxidative damage to the heart with an unequal intracellular distribution. Compared to the liver and brain the modifications caused by Arthritis in the heart are less pronounced on variables such as GSH levels and protein integrity. Possibly this occurs because the antioxidant system of the heart is less impaired by Arthritis than that reported for the former tissues. Even so, the modifications caused by Arthritis represent an imbalanced situation that probably contributes to the cardiac symptoms of the Arthritis disease.
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Oxidative state and oxidative metabolism in the brain of rats with Adjuvant-Induced Arthritis.
Experimental and molecular pathology, 2015Co-Authors: Mariana Marques Nogueira Wendt, Anacharis Babeto De Sá-nakanishi, Rosane Marina Peralta, Adelar Bracht, Cristiane Vizioli De Castro Ghizoni, Ciomar Aparecida Bersani Amado, Jurandir Fernando ComarAbstract:The purpose of the present study was to evaluate the oxidative status of the brain of arthritic rats, based mainly on the observation that Arthritis induces a pronounced oxidative stress in the liver of Arthritis rats and that morphological alterations have been reported to occur in patients with rheumatoid Arthritis. Rats with Adjuvant-Induced Arthritis were used. These animals presented higher levels of reactive oxygen species (ROS) in the total brain homogenate (25% higher) and in the mitochondria (+55%) when compared to healthy rats. The nitrite plus nitrate contents, nitric oxide (NO) markers, were also increased in both mitochondria (+27%) and cytosol (+14%). Arthritic rats also presented higher levels of protein carbonyl groups in the total homogenate (+43%), mitochondria (+69%) and cytosol (+145%). Arthritis caused a diminution of oxygen consumption in isolated brain mitochondria only when ascorbate was the electron donor. The disease diminished the mitochondrial cytochrome c oxidase activity by 55%, but increased the transmembrane potential by 16%. The pro-oxidant enzyme xanthine oxidase was 150%, 110% and 283% higher, respectively, in the brain homogenate, mitochondria and cytosol of arthritic animals. The same occurred with the calcium-independent NO-synthase activity that was higher in the brain homogenate (90%) and cytosol (122%) of arthritic rats. The catalase activity, on the other hand, was diminished by Arthritis in all cellular fractions (between 30 and 40%). It is apparent that the brain of rats with Adjuvant-Induced Arthritis presents a pronounced oxidative stress and a significant injury to lipids and proteins, a situation that possibly contributes to the brain symptoms of the Arthritis disease.
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oxidative state of the liver of rats with adjuvant induced Arthritis
Free Radical Biology and Medicine, 2013Co-Authors: Jurandir Fernando Comar, Mariana Marques Nogueira Wendt, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Anacharis Babeto De Sanakanishi, Andrea Luiza De Oliveira, Emy Luiza Ishii Iwamoto, Adelar BrachtAbstract:Adjuvant-Induced Arthritis is an experimental immunopathology in rats that is often used as a model for studying autoimmune chronic inflammation and inflammatory cachexia. In these animals oxidative stress is quite pronounced in the articular inflammation sites. The purpose of this study was to evaluate oxidative stress in the liver of arthritic rats in which morphological and metabolic alterations have been reported to occur. Oxidative injury parameters, levels and production of reactive oxygen species (ROS), and antioxidant parameters were measured in the total liver homogenate and in subcellular fractions, namely cytosol, mitochondria, and peroxisomes. Arthritic rats presented higher levels of ROS than controls in the total homogenate (46% higher) and in all subcellular fractions (51, 38, and 55% higher for mitochondria, peroxisome, and cytosol, respectively). Arthritic rats also presented higher levels of protein carbonyl groups in the total homogenate (75%) and in all subcellular fractions (189, 227, and 260%, respectively, for mitochondria, peroxisomes, and cytosol). The TBARS levels of arthritic rats were more elevated in the total homogenate (36%), mitochondria (20%), and peroxisomes (16%). Arthritic rats also presented higher levels of NO markers in the peroxisomes (112%) and in the cytosol (35%). The catalase activity of all cell compartments was strongly diminished (between 77 and 87%) by Arthritis, and glutathione peroxidase activities were diminished in the mitochondria (33.7%) and cytosol (41%). The cytosolic glucose-6-phosphate dehydrogenase activity, on the other hand, was increased (62.9%), the same happening with inducible peroxisomal NO synthase (119.3%). The superoxide dismutase and glutathione reductase activities were not affected. The GSH content was diminished by Arthritis in all cellular compartments (50 to 59% diminution). The results reveal that the liver of rats with Adjuvant-Induced Arthritis presents a pronounced oxidative stress and that, in consequence, injury to lipids and proteins is highly significant. The higher ROS content of the liver of arthritic rats seems to be the consequence of both a stimulated pro-oxidant system and a deficient antioxidant defense with a predominance of the latter as indicated by the strongly diminished activities of catalase and glutathione peroxidase.
