Papel protetor do ácido tânico sobre alterações oxidativas observadas na hipermetioninemia aguda em ratos

Abstract

Hypermethioninemia is characterized by high plasma concentrations of methionine (Met) and its metabolites such as methionine sulfoxide (MetO). Hypermethioninemic patients may present neurological and hepatic symptoms, which the treatment is based on a Met-free diet and supplementation with S-adenosylmethionine. In this context, natural compounds can be promising targets in clinical management and prevention of changes found in this pathology, such as tannic acid (TA), known to have antioxidant and neuroprotective action. Thus, the aim of this work was to investigate the ability of TA to prevent oxidative and nitrosative damage in the brain, liver, kidney and serum from rats submitted to an acute hypermethioninemia model. Male Wistar rats (23 days old) were divided into four groups: I - control, II - TA (30 mg/kg), III - Met (0.4 g/kg) + MetO (0.1 g/kg) and IV - TA + Met + MetO. The rats of groups II and IV received TA orally for seven days, and the rats of groups I and III received an equal volume of water. After pretreatment with TA, rats of groups II and IV received a single subcutaneous injection of Met + MetO and were euthanized 3 hours later. In brain structures (cerebral cortex, hippocampus and striatum) and in kidney, Met + MetO increased the levels of reactive oxygen species (ROS), nitrite and induced lipid peroxidation, followed by a reduction in the thiol content and in the activity of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST). On the other hand, pretreatment with TA prevented oxidative and nitrosative damage found in brain structures and kidney. In liver, there was a reduction in the levels of ROS and an increase in the total thiol content, which was accompanied by a reduction in the activities of CAT and GPx in the Met + MetO group, however pretreatment with TA was able to prevent the reduction in CAT activity. In serum, Met + MetO increased ROS levels and decreased the activity of antioxidant enzymes SOD and CAT, but the pretreatment with TA was able to prevent this reduction. Our results demonstrated that the administration of Met + MetO caused oxidative and nitrosative damage in the acute hypermethioninemia model; however, TA was able to prevent most of these changes, which makes it a possible adjunctive therapeutic alternative in the treatment of hypermethioninemia.