Potential effects of Eugenia uniflora fruits on the prevention of neurochemical and behavioral alterations in animal model of chronic unpredictable stress

Depression is one of the most common psychiatric disorders, and depression is a relatively common psychiatric disorder associated with significant morbidity and mortality. Despite the large number of pharmacological treatments, the success rate of antidepressants is not greater than 50-60%. So, the objective of this work was to evaluate the effect of chronic administration of Eugenia uniflora fruit extract on behavioral parameters, oxidative stress markers and acetylcholinesterase activity in an animal model of depression induced by chronic unpredictable stress (CUS). Our results showed that E. uniflora treatment prevented the depressant-like effect induced by CUS. Additionally, the extract regulated the activity of acetylcholinesterase, reduced lipid peroxidation and reactive oxygen species in the prefrontal cortex and hippocampus from animals submitted to CUS protocol. This extract was able to prevent the reduction of antioxidant enzyme glutathione peroxidase in the hippocampus. Total thiol content was decreased by CUS only in this cerebral structure and fruit extract was not able to block this alteration. However, no change was observed in the superoxide dismutase activity in the prefrontal cortex and hippocampus. Taken together, our findings suggest a neuroprotective effect of E. uniflora by preventing the depressive-type behavior, oxidative damage and increased CUS-induced acetylcholinesterase activity. Furthermore, our data provide further evidence of the importance of acetylcholinesterase and oxidative stress in the pathophysiology of depression.Sem bolsaA depressão é um transtorno psiquiátrico relativamente comum, associado com significativa morbidade e mortalidade. Apesar do grande número de tratamentos farmacológicos, a taxa de sucesso dos antidepressivos não é maior que 50-60%. Desta forma, é de grande interesse a busca por novas terapias que possam auxiliar no tratamento desta doença. Considerando o exposto, o objetivo deste trabalho foi avaliar o efeito da administração crônica de extrato de frutos de Eugenia uniflora (pitanga) em parâmetros comportamentais, de estresse oxidativo e na atividade da acetilcolinesterase em córtex pré-frontal e hipocampo de animais submetidos ao modelo de depressão induzida pelo estresse crônico imprevisível (ECI). Nossos resultados demonstraram que o tratamento com pitanga preveniu o efeito tipo depressivo induzido pelo ECI. Adicionalmente, o extrato de E. uniflora regulou a atividade da acetilcolinesterase, reduziu a lipoperoxidação e a produção de espécies reativas de oxigênio tanto em córtex pré-frontal quanto em hipocampo de animais submetidos ao ECI. Ainda, foi capaz de prevenir a redução na atividade da enzima antioxidante glutationa peroxidase em hipocampo. O conteúdo tiólico total foi reduzido pelo ECI somente nesta estrutura e o extrato não foi capaz de impedir esta alteração. Nenhuma modificação foi observada na atividade da enzima superóxido dismutase nas duas estruturas cerebrais testadas. Em conjunto, nossos achados sugerem um efeito neuroprotetor da pitanga por prevenir o comportamento tipo depressivo, dano oxidativo e aumento da atividade da acetilcolinesterase induzidos pelo ECI. E ainda, nossos dados fornecem mais evidências da importância da acetilcolinesterase e estresse oxidativo na fisiopatologia da depressão

Methionine and methionine sulfoxide alter parameters of oxidative stress in the liver of young rats : in vitro and in vivo studies

It has been shown that elevation of plasma methionine (Met) and its metabolites may occur in several genetic abnormalities. In this study we investigated the in vitro and in vivo effects of the Met and methionine sulfoxide (MetO) on oxidative stress parameters in the liver of rats. For in vitro studies, liver homogenates were incubated with Met, MetO, and Mix (Met + MetO). For in vivo studies, the animals were divided into groups: saline, Met 0.4 g/kg, MetO 0.1 g/kg, and Met 0.4 g/kg + MetO 0.1 g/kg. The animals were euthanized 1 and 3 h after injection. In vitro results showed that Met 1 and 2 mM and Mix increased catalase (CAT) activity. Superoxide dismutase (SOD) was enhanced by Met 1 and 2 mM, MetO 0.5 mM, and Mix. Dichlorofluorescein oxidation was increased by Met 1 mM and Mix. In vivo results showed that Met, MetO, and Mix decreased TBARS levels at 1 h. Total thiol content decreased 1 h after and increased 3 h after MetO and Met plus MetO administrations. Carbonyl content was enhanced by Met and was reduced by MetO 1 h after administration. Met, MetO and Met plus MetO decreased CAT activity 1 and 3 h after administration. Furthermore, only MetO increased SOD activity. In addition, Met, MetO, and Mix decreased dichlorofluorescein oxidation at 1 and 3 h. Our data indicate that Met/MetO in vivo and in vitro modify liver homeostasis by altering the redox cellular state. However, the hepatic changes caused by these compounds suggest a short-time adaptation of this tissue