Eritroleucometria, perfil bioquímico, glicemia, histoptologia e estresse oxidativo em ratos Wistar diabéticos infectados com Trypanosoma evansi

• Autor(a) principal: Morales, Carla Orloski [UNESP]
• Data de Publicação: 2015
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://hdl.handle.net/11449/149244; http://www.athena.biblioteca.unesp.br/exlibris/bd/cathedra/02-02-2017/000878429.pdf
• topic: Diabetes mellitus; Antioxidantes; Infecção; Tripanossomose; Ratos Wistar; Antioxidants; Infection

Trypanosoma evansi has extensive worldwide distribution, occurring in Africa, Asia, Europe, Central and South America in infects horses, cattle, dogs, cats, small ruminants, camels, capybaras, coatis, deer and rabbits. T. evansi is avid consumer of plasma glucose, causes severe hypoglycemia, commonly found in infected animals. Diabetes is characterized by persistent hyperglycemia maintenance, which leads to oxidative stress, and induces the majority of diabetic complications. The objective of this study was to observe the influence of T. evansi in oxidative stress in diabetic Wistar rats and in red and white cells counts, biochemical profile and verify histopathological changes resulting from the experimental infection. Forty rats were divided into four groups, uninfected group and not diabetic (GC), diabetic group (GD), infected group (GI) and diabetic and infected group (GDI). GD kept higher oxidation rates compared to the GDI and GI, indicating that the parasite infection favoring a decrease in oxidative stress caused by diabetes model proposed. A significant reduction of all hematological parameters, except for the VCM, was observed. Hyperglycemia inherent in the diabetic status, induced by streptozotocin may have triggered a non-alcoholic hepatic steatosis condition in the diabetic group, as indicated by elevated serum levels of AST and ALT. Thus, infection with T. evansi in GDI could have protected individuals of developing such a condition