Ameliorative effect of tannic acid on hypermethioninemia-induced oxidative and nitrosative damage in rats: biochemical-based evidences in liver, kidney, brain, and serum

We investigated the ability of tannic acid (TA) to prevent oxidative and nitrosative damage in the brain, liver, kidney, and serum of a rat model of acute hypermethioninemia. Young Wistar rats were divided into four groups: I (control), II (TA 30 mg/kg), III (methionine (Met) 0.4 g/kg + methionine s...

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Veröffentlicht in:Amino acids 2020-12, Vol.52 (11-12), p.1545-1558
Hauptverfasser: de Moraes Meine, Bernardo, Bona, Natália Pontes, Luduvico, Karina Pereira, de Souza Cardoso, Juliane, Spohr, Luiza, de Souza, Anita Ávila, Spanevello, Roselia Maria, Soares, Mayara Sandrielly Pereira, Stefanello, Francieli Moro
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container_end_page 1558
container_issue 11-12
container_start_page 1545
container_title Amino acids
container_volume 52
creator de Moraes Meine, Bernardo
Bona, Natália Pontes
Luduvico, Karina Pereira
de Souza Cardoso, Juliane
Spohr, Luiza
de Souza, Anita Ávila
Spanevello, Roselia Maria
Soares, Mayara Sandrielly Pereira
Stefanello, Francieli Moro
description We investigated the ability of tannic acid (TA) to prevent oxidative and nitrosative damage in the brain, liver, kidney, and serum of a rat model of acute hypermethioninemia. Young Wistar rats were divided into four groups: I (control), II (TA 30 mg/kg), III (methionine (Met) 0.4 g/kg + methionine sulfoxide (MetO) 0.1 g/kg), and IV (TA/Met + MetO). Rats in groups II and IV received TA orally for seven days, and rats of groups I and III received an equal volume of water. After pretreatment with TA, rats from groups II and IV received a single subcutaneous injection of Met + MetO, and were euthanized 3 h afterwards. In specific brain structures and the kidneys, we observed that Met + MetO led to increased reactive oxygen species (ROS), nitrite, and lipid peroxidation levels, followed by a reduction in thiol content and antioxidant enzyme activity. On the other hand, pretreatment with TA prevented both oxidative and nitrosative damage. In the serum, Met + MetO caused a decrease in the activity of antioxidant enzymes, which was again prevented by TA pretreatment. In contrast, in the liver, there was a reduction in ROS levels and an increase in total thiol content, which was accompanied by a reduction in catalase and superoxide dismutase activities in the Met + MetO group, and pretreatment with TA was able to prevent only the reduction in catalase activity. Conclusively, pretreatment with TA has proven effective in preventing oxidative and nitrosative changes caused by the administration of Met + MetO, and may thus represent an adjunctive therapeutic approach for treatment of hypermethioninemia.
doi_str_mv 10.1007/s00726-020-02913-5
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Young Wistar rats were divided into four groups: I (control), II (TA 30 mg/kg), III (methionine (Met) 0.4 g/kg + methionine sulfoxide (MetO) 0.1 g/kg), and IV (TA/Met + MetO). Rats in groups II and IV received TA orally for seven days, and rats of groups I and III received an equal volume of water. After pretreatment with TA, rats from groups II and IV received a single subcutaneous injection of Met + MetO, and were euthanized 3 h afterwards. In specific brain structures and the kidneys, we observed that Met + MetO led to increased reactive oxygen species (ROS), nitrite, and lipid peroxidation levels, followed by a reduction in thiol content and antioxidant enzyme activity. On the other hand, pretreatment with TA prevented both oxidative and nitrosative damage. In the serum, Met + MetO caused a decrease in the activity of antioxidant enzymes, which was again prevented by TA pretreatment. In contrast, in the liver, there was a reduction in ROS levels and an increase in total thiol content, which was accompanied by a reduction in catalase and superoxide dismutase activities in the Met + MetO group, and pretreatment with TA was able to prevent only the reduction in catalase activity. Conclusively, pretreatment with TA has proven effective in preventing oxidative and nitrosative changes caused by the administration of Met + MetO, and may thus represent an adjunctive therapeutic approach for treatment of hypermethioninemia.</abstract><cop>Vienna</cop><pub>Springer Vienna</pub><pmid>33184691</pmid><doi>10.1007/s00726-020-02913-5</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-2181-3591</orcidid></addata></record>
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source SpringerNature Journals
subjects Analytical Chemistry
Animal models
Antioxidants
Biochemical Engineering
Biochemistry
Biomedical and Life Sciences
Brain damage
Brain injury
Catalase
Damage prevention
Enzymatic activity
Enzyme activity
Kidneys
Life Sciences
Lipid peroxidation
Lipids
Liver
Methionine
Neurobiology
Original Article
Pretreatment
Proteomics
Reactive oxygen species
Rodents
Superoxide dismutase
Tannic acid
title Ameliorative effect of tannic acid on hypermethioninemia-induced oxidative and nitrosative damage in rats: biochemical-based evidences in liver, kidney, brain, and serum
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