Ameliorative effect of tannic acid on hypermethioninemia-induced oxidative and nitrosative damage in rats: biochemical-b
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ORIGINAL ARTICLE
Ameliorative effect of tannic acid on hypermethioninemia‑induced oxidative and nitrosative damage in rats: biochemical‑based evidences in liver, kidney, brain, and serum Bernardo de Moraes Meine1 · Natália Pontes Bona1 · Karina Pereira Luduvico1 · Juliane de Souza Cardoso1 · Luiza Spohr2 · Anita Ávila de Souza2 · Roselia Maria Spanevello2 · Mayara Sandrielly Pereira Soares2 · Francieli Moro Stefanello1 Received: 26 June 2020 / Accepted: 6 November 2020 © Springer-Verlag GmbH Austria, part of Springer Nature 2020
Abstract 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. Keywords Redox status · Prevention · Natural product · Tissue damage · Acute hypermethioninemia
Introduction
Handling Editor: E. Agostinelli. * Mayara Sandrielly Pereira Soares [email protected] 1
Programa de Pós‑Graduação em Bioquímica e Bioprospecção, Laboratório de Biomarcadores, Centro de Ciências Químicas, Farmacêuticas e de Alimentos, Universidade Federal de Pelotas, Campus Universitário s/n, Pelotas, RS, Brazil
Programa de Pós‑Graduação em Bioquímica e Bioprospecção, Laboratório de Neuroquímica, Inflamação e Câncer, Centro de Ciências Químicas, Farmacêuticas e de Alimentos, Universidade Federal de Pelotas, Campus Universitário s/n, Pelotas, RS 96010‑900, Brazil
2
Methionine (Met) is an essential sulfur-containing amino acid necessary for normal healthy growth (Chiang et al. 1996). However, elevation of Met body levels due to the accumulation of Met and/or methioni
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