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The present study investigated whether and to what extent caffeine chronic use can influence the brain oxidative status and the behavioral activity of the C57BL/6 female mice. For this, fifteen animals were randomized in the following groups: Control, Caf10: 10 mg/kg caffeine, and Caf50: 50 mg/kg caffeine. The animals received one daily caffeine dose by i.p route by 120 days. Twenty-four hours after the last administration, the animals were subjected to behavioral tests and euthanized. The blood was used by biochemical analysis and the brain to evaluate the oxidative status and micromineral levels. The caffeine does not influence the anthropometric parameters, lipid profile, and the C-reactive protein levels. In the same way, SOD and glutathione-s-transferase (GST) activities maintained the same response profile. On the other hand, catalase (CAT) activity was decreased in both groups receiving caffeine. Despite this, malondialdehyde and carbonyl protein levels did not change among the groups, as well as the distribution of the chemical elements. In the same way, none caffeine dose was caused increased anxiety degree in the animals. Considering the time of caffeine administration, we believe that there was the cellular adaptation triggered by its use, tending to a protective effect on the brain. Amplamente consumida nos alimentos e como suplemento alimentar, a cafeína tem sido estudada devido aos seus efeitos farmacológicos, principalmente no sistema nervoso central (SNC). O presente estudo investigou se o uso crônico da cafeína pode influenciar o estado oxidativo do cérebro e a atividade comportamental de camundongos fêmeas C57BL/6. Para isso, quinze animais foram randomizados nos seguintes grupos: Controle (solução salina à 0,9%), Caf10 (10 mg / kg de cafeína) e Caf50 (50 mg / kg de cafeína). Os animais receberam uma dose diária de cafeína por via i.p. durante 120 dias. Vinte e quatro horas após a última administração, os animais foram submetidos a testes comportamentais e foram eutanasiados. O sangue foi utilizado para análises bioquímicas. No cérebro, foi avaliado o estado oxidativo e os níveis de microminerais. A cafeína não influenciou os parâmetros antropométricos, perfil lipídico e níveis de proteína Creativa. Ademais, as atividades de superóxido dismutase (SOD) e glutationa-Stransferase (GST) mantiveram o mesmo perfil de resposta. Em contrapartida, a atividade da catalase (CAT) diminuiu em ambos os grupos que receberam cafeína. Já os níveis de malondialdeído e proteína carbonilada não se alteraram entre os grupos, assim como a distribuição dos microminerais. Nenhuma dose de cafeína desencadeou comportamento do tipo ansioso nos animais. Portanto, considerando o tempo de administração da cafeína, acreditamos que houve a adaptação celular desencadeada pelo seu uso, tendendo a um efeito protetor no cérebro. Além disso, o espaço amostral reduzido foi uma limitação para entendimentos mais acurados sobre os efeitos da cafeína no SNC. Palavras-chave: Cafeína. Espécies reativas de oxigênio. Comportamento Animal.

Background and Aims: Recent studies have proposed that if a severe caloric restriction (SCR) is initiated at the earliest period of postnatal life, it can lead to beneficial cardiac adaptations later on. We investigated the effects of SCR in Wistar rats from birth to adult age on risk factors for cardiac diseases (CD), as well as cardiac function, redox status, and HSP72 content in response to ischemia/reperfusion (I/R) injury. Methods and Results: From birth to the age of 3 months, CR50 rats were fed 50% of the food that the ad libitum group (AL) was fed. Food intake was assessed daily and body weight were assessed weekly. In the last week of the SCR protocol, systolic blood pressure and heart rate were measured and the double product index was calculated. Also, oral glucose and intraperitoneal insulin tolerance tests were performed. Thereafter, rats were decapitated, visceral fat was weighed, and blood and hearts were harvested for biochemical, functional, tissue redox status, and western blot analyzes. Compared to AL, CR50 rats had reduced the main risk factors for CD. Moreover, the FR50 rats showed increased cardiac function both at baseline conditions (45% > AL rats) and during the post-ischemic period (60% > AL rats) which may be explained by a decreased cardiac oxidative stress and increased HSP72 content. Conclusion: SCR from birth to adult age reduced risk factors for CD, increased basal cardiac function and protected hearts from the I/R, possibly by a mechanism involving ROS.