Oxidative state and oxidative metabolism in the brain of rats with adjuvant-induced arthritis

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 rh...

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Veröffentlicht in:Experimental and molecular pathology 2015-06, Vol.98 (3), p.549-557
Hauptverfasser: Wendt, Mariana Marques Nogueira, de Sá-Nakanishi, Anacharis Babeto, de Castro Ghizoni, Cristiane Vizioli, Bersani Amado, Ciomar Aparecida, Peralta, Rosane Marina, Bracht, Adelar, Comar, Jurandir Fernando
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container_issue 3
container_start_page 549
container_title Experimental and molecular pathology
container_volume 98
creator Wendt, Mariana Marques Nogueira
de Sá-Nakanishi, Anacharis Babeto
de Castro Ghizoni, Cristiane Vizioli
Bersani Amado, Ciomar Aparecida
Peralta, Rosane Marina
Bracht, Adelar
Comar, Jurandir Fernando
description 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. •The brain of arthritic rats presents pronounced oxidative stress.•There is considerable injury to lipids and proteins.•The causes are increased production of reactive species and impaired defense.•This situation possibly contributes to the brain symptoms of arthritis disease.
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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%). 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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. •The brain of arthritic rats presents pronounced oxidative stress.•There is considerable injury to lipids and proteins.•The causes are increased production of reactive species and impaired defense.•This situation possibly contributes to the brain symptoms of arthritis disease.</description><subject>Adjuvant arthritis</subject><subject>Animals</subject><subject>Antioxidant enzymes</subject><subject>Arthritis, Experimental - metabolism</subject><subject>Brain - metabolism</subject><subject>Brain oxidative state</subject><subject>Chronic inflammation</subject><subject>Lipid Metabolism</subject><subject>Male</subject><subject>Mitochondria - metabolism</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Oxidative Stress</subject><subject>Rats</subject><subject>Reactive oxygen and nitrogen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Xanthine Oxidase - metabolism</subject><issn>0014-4800</issn><issn>1096-0945</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1P3DAQhq2qVVlof0El5GMvCTOJE8eHHhCigITEpT1Wlj8mWq82yWI7C_z7ZruUI6cZjZ53RvMw9g2hRMD2YlO-0POwKyvApgRRAlQf2ApBtQUo0XxkKwAUhegATthpShsAUIDVZ3ZSNZ08MCv25-E5eJPDnnjKJhM3o-fT22ygbOy0DWngYeR5TdxGs3RTz6PJiT-FvObGb-a9GXMRRj878tzEvI4hh_SFferNNtHX13rGfv-8_nV1W9w_3NxdXd4Xrm5ULlylrGhAeVJItWrRKuy9FK3tsKNaQk1OSpTSNr71wvZka0HYSkHKGSPrM_b9uHcXp8eZUtZDSI62WzPSNCeNbYdVi6KpF7Q-oi5OKUXq9S6GwcQXjaAPXvVG__OqD141CL14XVLnrwdmO5B_y_wXuQA_jgAtb-4DRZ1coHGxESK5rP0U3j3wFyD0i4o</recordid><startdate>201506</startdate><enddate>201506</enddate><creator>Wendt, Mariana Marques Nogueira</creator><creator>de Sá-Nakanishi, Anacharis Babeto</creator><creator>de Castro Ghizoni, Cristiane Vizioli</creator><creator>Bersani Amado, Ciomar Aparecida</creator><creator>Peralta, Rosane Marina</creator><creator>Bracht, Adelar</creator><creator>Comar, Jurandir Fernando</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201506</creationdate><title>Oxidative state and oxidative metabolism in the brain of rats with adjuvant-induced arthritis</title><author>Wendt, Mariana Marques Nogueira ; 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subjects Adjuvant arthritis
Animals
Antioxidant enzymes
Arthritis, Experimental - metabolism
Brain - metabolism
Brain oxidative state
Chronic inflammation
Lipid Metabolism
Male
Mitochondria - metabolism
Nitric Oxide Synthase - metabolism
Oxidative Stress
Rats
Reactive oxygen and nitrogen species
Reactive Oxygen Species - metabolism
Xanthine Oxidase - metabolism
title Oxidative state and oxidative metabolism in the brain of rats with adjuvant-induced arthritis
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