Chemical hypermethioninemia in young mice: oxidative damage and reduction of antioxidant enzyme activity in brain, kidney, and liver

التفاصيل البيبلوغرافية
العنوان: Chemical hypermethioninemia in young mice: oxidative damage and reduction of antioxidant enzyme activity in brain, kidney, and liver
المؤلفون: Bernardo de Moraes Meine, Thaís Scolari Franceschi, Natália Pontes Bona, Luiza Spohr, Nathalia Stark Pedra, Roselia Maria Spanevello, Mayara Sandrielly Soares de Aguiar, Francieli Moro Stefanello
المصدر: Metabolic brain disease.
سنة النشر: 2022
مصطلحات موضوعية: Cellular and Molecular Neuroscience, Neurology (clinical), Biochemistry
الوصف: High levels of methionine (Met) and its metabolites, such as methionine sulfoxide (MetO), found in hypermethioninemia, can be detrimental to the body; however, the underlying mechanisms are still uncertain. Using a recently standardized protocol, the aim of this study was to investigate the effects of chronic administration of Met and/or MetO on parameters of oxidative damage in the total brain, liver, and kidney of young mice. Swiss male mice were subcutaneously injected with Met and MetO at concentrations of 0.35–1.2 g/kg body weight and 0.09–0.3 g/kg body weight, respectively, from the 10th − 38th day post-birth, while the control group was treated with saline solution. Results showed that Met and/or MetO caused an increase in reactive oxygen species (ROS) and lipoperoxidation, along with a reduction of superoxide dismutase (SOD) and catalase (CAT) activities in the brain. In the liver, Met and/or MetO enhanced ROS and nitrite levels, and reduced SOD, CAT, and delta aminolevulinic dehydratase activities. The effects on the kidney were an increase in ROS production and SOD activity, and a reduction in thiol content and CAT activity. These data demonstrated the contribution of redox imbalance to the systemic changes found in patients with hypermethioninemia. In conclusion, our findings may help future studies to better understand the pathophysiological mechanisms of hypermethioninemia as well as contribute to the search for new therapeutic agents for this pathology.
تدمد: 1573-7365
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::68edb05eeb361c4659098018b889e092
https://pubmed.ncbi.nlm.nih.gov/36308587
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....68edb05eeb361c4659098018b889e092
قاعدة البيانات: OpenAIRE