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Adjuvant-Induced Arthritis

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Jurandir Fernando Comar – One of the best experts on this subject based on the ideXlab platform.

  • Oxidative state and oxidative metabolism of the heart from rats with Adjuvant-Induced Arthritis.
    Experimental and molecular pathology, 2016
    Co-Authors: Amanda Caroline Schubert, Mariana Marques Nogueira Wendt, Anacharis Babeto De Sá-nakanishi, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Jurandir Fernando Comar, Adelar Bracht
    Abstract:

    The aim of the present work was to investigate, in a more extensive way, the oxidative state and parameters related to energy metametabolism 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.

  • Oxidative state and oxidative metabolism in the brain of rats with Adjuvant-Induced Arthritis.
    Experimental and Molecular Pathology, 2015
    Co-Authors: Mariana Marques Nogueira Wendt, Adelar Bracht, Anacharis Babeto De Sá-nakanishi, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Cristiane Vizioli De Castro Ghizoni, Jurandir Fernando Comar
    Abstract:

    The aim of the present work was to investigate, in a more extensive way, the oxidative state and parameters related to energy metametabolism 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.

  • Oxidative state and oxidative metabolism in the brain of rats with Adjuvant-Induced Arthritis.
    Experimental and molecular pathology, 2015
    Co-Authors: Mariana Marques Nogueira Wendt, Adelar Bracht, Anacharis Babeto De Sá-nakanishi, Rosane Marina Peralta, Cristiane Vizioli De Castro Ghizoni, Ciomar Aparecida Bersani Amado, Jurandir Fernando Comar
    Abstract:

    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.

Adelar Bracht – One of the best experts on this subject based on the ideXlab platform.

  • Oxidative state and oxidative metabolism of the heart from rats with Adjuvant-Induced Arthritis.
    Experimental and molecular pathology, 2016
    Co-Authors: Amanda Caroline Schubert, Mariana Marques Nogueira Wendt, Anacharis Babeto De Sá-nakanishi, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Jurandir Fernando Comar, Adelar Bracht
    Abstract:

    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.

  • Oxidative state and oxidative metabolism in the brain of rats with Adjuvant-Induced Arthritis.
    Experimental and Molecular Pathology, 2015
    Co-Authors: Mariana Marques Nogueira Wendt, Adelar Bracht, Anacharis Babeto De Sá-nakanishi, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Cristiane Vizioli De Castro Ghizoni, Jurandir Fernando Comar
    Abstract:

    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.

  • Oxidative state and oxidative metabolism in the brain of rats with Adjuvant-Induced Arthritis.
    Experimental and molecular pathology, 2015
    Co-Authors: Mariana Marques Nogueira Wendt, Adelar Bracht, Anacharis Babeto De Sá-nakanishi, Rosane Marina Peralta, Cristiane Vizioli De Castro Ghizoni, Ciomar Aparecida Bersani Amado, Jurandir Fernando Comar
    Abstract:

    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.

Andrew H. Kang – One of the best experts on this subject based on the ideXlab platform.

Jeanmarie Besson – One of the best experts on this subject based on the ideXlab platform.

  • c fos expression in rat lumbar spinal cord during the development of adjuvant induced Arthritis
    Neuroscience, 1992
    Co-Authors: C Abbadie, Jeanmarie Besson
    Abstract:

    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 protooncogene 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 inflinflammation 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 inflinflammatory 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.

  • Oxidative state and oxidative metabolism of the heart from rats with Adjuvant-Induced Arthritis.
    Experimental and molecular pathology, 2016
    Co-Authors: Amanda Caroline Schubert, Mariana Marques Nogueira Wendt, Anacharis Babeto De Sá-nakanishi, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Jurandir Fernando Comar, Adelar Bracht
    Abstract:

    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.

  • Oxidative state and oxidative metabolism in the brain of rats with Adjuvant-Induced Arthritis.
    Experimental and Molecular Pathology, 2015
    Co-Authors: Mariana Marques Nogueira Wendt, Adelar Bracht, Anacharis Babeto De Sá-nakanishi, Ciomar Aparecida Bersani Amado, Rosane Marina Peralta, Cristiane Vizioli De Castro Ghizoni, Jurandir Fernando Comar
    Abstract:

    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.

  • Oxidative state and oxidative metabolism in the brain of rats with Adjuvant-Induced Arthritis.
    Experimental and molecular pathology, 2015
    Co-Authors: Mariana Marques Nogueira Wendt, Adelar Bracht, Anacharis Babeto De Sá-nakanishi, Rosane Marina Peralta, Cristiane Vizioli De Castro Ghizoni, Ciomar Aparecida Bersani Amado, Jurandir Fernando Comar
    Abstract:

    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.