Fernanda Bonatto

Recognition memory impairment and brain oxidative stress induced by postnatal iron administration.

Iron accumulation in the brain has been implicated in the pathogenesis of neurodegenerative disorders. It is known that iron catalyses the formation of highly reactive hydroxyl radicals. Recent studies have implicated oxidative damage in memory deficits in rats and humans. The purpose of the present study was to investigate the long‐term effects of iron treatment in four different phases of the neonatal period on recognition memory in rats. Additionally, parameters of oxidative stress in cerebral regions related to memory formation were evaluated. Male Wistar rats received vehicle or 10.0 mg/kg of Fe2+ orally at postnatal days 5–7, 12–14, 19–21 or 30–32. Animals given iron at any phase of the neonatal period showed impairments in long‐term retention of object recognition memory, although only the group given iron from postnatal days 12–14 showed a complete memory blockade. Iron treatment induced oxidative damage in the brain as assessed by the thiobarbituric acid reactive species assay. Moreover, iron administration increased superoxide production in submitochondrial particles, suggesting impaired mitochondrial function; and there was an increase in superoxide dismutase activity in brain regions susceptible to iron administration. The results show that iron load in the early stages of life induces cognitive impairment possibly by inducing oxidative damage in the brain. These findings are consistent with the view that oxidative stress may be related to the cognitive decline observed in normal ageing.

Effect of protein malnutrition on redox state of the hippocampus of rat

The protein malnutrition is a worldwide problem, affecting mainly newborns and children of developing countries. This deficiency reaches the brain in the most critical period of the development. Various consequences are related to this insult, such as memory disturbance, learning, and behavioral impairment. Protein content of the diet plays an important role on antioxidant mechanisms. This study observed the effects of protein malnutrition on rat hippocampus redox state. Wistar rats were separate in four groups, receiving different diets: first group with 25% casein, protein deficient group with 8% casein, and the same two groups supplemented with methionine (0.15%). Diets were isocaloric and were administered since the prenatal period up to the sacrifice. Rats were decapitated at 21 or 75 days old and hippocampus were isolated for measuring the lipoperoxidation by TBARS method, protein oxidative damage by carbonyl (DNPH) levels, and the activities of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). There was significant alterations in the activities of the enzyme SOD, lipoperoxidation, and protein oxidation in hippocampus of 21 and 75 day-old rats fed with 25% of protein with methionine and the groups fed with low levels of protein (8%) both supplemented or not with methionine. Our data suggest that both the content of protein in the diet and the essential amino acid methionine may alter the antioxidant system and the redox state of the brain.

Structure-related oxidative damage in rat brain after acute and chronic electroshock

The role of oxidative stress in electroconvulsive therapy–related effects is not well studied. The purpose of this study was to determine oxidative stress parameters in several brain structures after a single electroconvulsive seizure or multiple electroconvulsive seizures. Rats were given either a single electroconvulsive shock or a series of eight electroconvulsive shocks. Brain regions were isolated, and levels of oxidative stress in the brain tissue (cortex, hippocampus, striatum and cerebellum) were measured. We demonstrated a decrease in lipid peroxidation and protein carbonyls in the hippocampus, cerebellum, and striatum several times after a single electroconvulsive shock or multiple electroconvulsive shocks. In contrast, lipid peroxidation increases both after a single electroconvulsive shock or multiple electroconvulsive shocks in cortex. In conclusion, we demonstrate an increase in oxidative damage in cortex, in contrast to a reduction of oxidative damage in hippocampus, striatum, and cerebellum.

No evidence for oxidative damage in the hippocampus after acute and chronic electroshock in rats

Although several advances has occurred over the past 20 years concerning the use of electroconvulsive therapy (ECT), little progress has been made in the mechanisms underlying its therapeutic or adverse effects. Thus, this work was performed in order to determine the level of oxidative damage and antioxidant enzyme activities early and late after acute and chronic electroconvulsive shock (ECS). We demonstrated a decrease in lipid peroxidation in the hippocampus immediately after and up to 30 days after a single or multiple electroconvulsive shock. This was also true for protein carbonyls in the acute protocol. We demonstrated an increase in catalase (CAT) and superoxide dismutase (SOD) activities at different time points after single and multiple electroconvulsive shock. Our findings, for the first time, demonstrated that after electroconvulsive shock, there is an increase in antioxidant enzyme activities and we cannot demonstrate oxidative damage in the hippocampus.

Effects of maternal protein malnutrition on oxidative markers in the young rat cortex and cerebellum

Malnutrition affects a large number of children worldwide. Inadequate nutrition during pre- and postnatal period may alter brain development resulting in biochemical, physiological and anatomical changes which in turn could cause behavioral abnormalities. The impairment of the central nervous system following protein deficit have been extensively studied and this deprivation produces deleterious effects upon cerebral structures. The aim of this study was to identify oxidative parameters present in the developing brain as consequence of maternal protein malnutrition. Female Wistar rats were fed a normal protein diet (25% casein) or low protein diet (8% casein) from the time of conception up to 21 days after the parturition. In addition, the diets were supplemented or not with l-methionine. Cortex and cerebellum were removed from offspring to determine the activity of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and the levels of lipoperoxidation (TBARS). Our findings demonstrated heterogeneity in response to protein restriction. The levels of lipoperoxidation were increased in the cerebellum of malnourished offspring. Methionine supplementation caused an increase in lipoperoxidation in both brain structures. CAT activity was decreased in the cerebellum of the offspring supplemented with methionine whereas the cerebellum of malnourished pups with or not methionine supplementation showed a decrease in SOD activity. The activity of SOD in the cortex did not differ among groups. CAT activity, however, was increased in the cortex of malnourished pups supplemented or not with methionine. Thus, these results provide clues to the knowledge of malnutrition effects upon the brain.

Avaliação de empreendimentos habitacionais de interesse social com base na hierarquia de valor percebido pelo usuário

A avaliacao de empreendimentos tem grande importância no esforco de melhoria da habitacao de interesse social, podendo auxiliar na avaliacao de resultados, e identificacao de erros e acertos frente aos objetivos e acoes do projeto. No entanto, a diversidade e dinâmica de programas habitacionais e a falta de clareza nos objetivos dos empreendimentos podem dificultar o processo de avaliacao desse tipo de produto. Com frequencia, as avaliacoes realizadas nos empreendimentos de habitacao de interesse social tem como foco os atributos do produto, sem estabelecer uma conexao com os objetivos esperados. Neste artigo, propoe-se um modelo para estruturar as avaliacoes de empreendimentos habitacionais de interesse social, adotando uma hierarquia de valor que vincula os atributos as suas consequencias de uso e aos objetivos esperados. O modelo nao esta limitado a um programa habitacional especifico e parte da ideia de produto ampliado, ou seja, nao esta focado apenas no produto habitacao. As principais contribuicoes do estudo referem-se ao mapeamento do produto habitacional e a identificacao de influencias entre os atributos do produto avaliados e os resultados esperados pelos gestores e percebidos pelos usuarios.

Oxidative damage in brains of mice treated with apomorphine and its oxidized derivative

Increasing evidence suggests that some of the neurobiological and neurotoxic actions of apomorphine and other dopamine receptor agonists might be mediated by their oxidation derivatives. The aim of the present study was to evaluate the effects of apomorphine and its oxidation derivative, 8-oxo-apomorphine-semiquinone (8-OASQ), on oxidative stress parameters and antioxidant enzyme activity. Adult male CF-1 mice were treated with a systemic injection of apomorphine (0.4, 4.0 or 40.0 mg/kg) or 8-OASQ (0.4, 4.0 or 40.0 mg/kg). Animals were sacrificed by decapitation 24 h after treatment, and the forebrains were collected for analysis of thiobarbituric acid reactive species, protein carbonyls, the total radical-trapping antioxidant parameter, catalase and superoxide dismutase. These treatments did not induce lipid peroxidation at any dose tested. In contrast, apomorphine induced an increase in protein carbonylation and a decrease in total radical-trapping antioxidant parameter at all doses tested. 8-OASQ induced an increase in protein carbonylation and a decrease in total radical-trapping antioxidant parameter only at the higher dose tested. All apomorphine doses tested induced an increase in catalase, but not superoxide dismutase activities. In contrast, 8-OASQ induced a dose-dependent increase in CAT activity. The results suggest that apomorphine and its oxidation product, 8-OASQ, induce differential effects on CNS oxidative parameters.