Effects of maintenance electroshock on the oxidative damage parameters in the rat brain.

Although several advances have occurred over the past 20 years concerning refining the use and administration of electroconvulsive therapy to minimize side effects of this treatment, little progress has been made in understanding the mechanisms underlying its therapeutic or adverse effects. This work was performed in order to determine the level of oxidative damage at different times after the maintenance electroconvulsive shock (ECS). Male Wistar rats (250-300 g) received a protocol mimicking therapeutic of maintenance or simulated ECS (Sham) and were subsequently sacrificed immediately after, 48 h and 7 days after the last maintenance electroconvulsive shock. We measured oxidative damage parameters (thiobarbituric acid reactive species for lipid peroxidation and protein carbonyls for protein damage, respectively) in hippocampus, cortex, cerebellum and striatum. We demonstrated no alteration in the lipid peroxidation and protein damage in the four structures studied immediately after, 48 h and 7 days after a last maintenance electroconvulsive shock. Our findings, for the first time, demonstrated that after ECS maintenance we did protocol minimal oxidative damage in the brain regions, predominating absence of damage on the findings.

Malathion-induced oxidative stress in rat brain regions.

Malathion is a pesticide with high potential for human exposure. However, it is possible that during the malathion metabolism, there is generation of reactive oxygen species (ROS) and malathion may produce oxidative stress in intoxicated rats. The present study was therefore undertaken to determine malathion-induced lipid peroxidation (LPO), protein carbonylation and to determine whether malathion intoxication alters the antioxidant system in brain rats. Malathion was administered intraperitoneally in the acute and chronic protocols in the doses of 25, 50, 100 and 150 mg malathion/kg. The results showed that LPO in brain increased in both protocols. The increased oxidative stress resulted in an increased in the activity of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT), observed in cortex, striatum in the acute malathion protocol and hippocampus in the chronic malathion protocol. Our results demonstrated that malathion induced oxidative stress and modulated SOD and CAT activity in selective brain regions.

Long lasting effects of electroconvulsive seizures on brain oxidative parameters.

This work was performed in order to determine the level of oxidative damage and antioxidant enzymes activities late after acute and chronic electroconvulsive shock (ECS) in rats. We measured oxidative parameters in hippocampus, cortex, and striatum, at 45, 60, 90 and 120 days after a single or multiple ECS. We demonstrated an increase in lipid peroxidation after multiple ECS in the hippocampus and striatum. This was also the case for protein carbonyls in the single or multiple protocols. In this way, we demonstrated an increase in catalase in cortex in contrast to striatum and hippocampus, were there were decreases sometimes in chronic ECS. The superoxide dismutase activities decrease in different times after single and multiple ECS in the hippocampus. Our findings demonstrated that there is a delayed increase after ECS in oxidative damage and decrease in antioxidant enzymes activities in hippocampus and striatum.

Oxidative variables in the rat brain after sepsis induced by cecal ligation and perforation.

OBJECTIVE: The underlying mechanisms of the changes in mental status, septic encephalopathy, and long-term cognitive symptoms in sepsis survivors have only been defined in part. The present study was undertaken to assess different variables of oxidative stress in several brain structures after cecal ligation and perforation in the rat. DESIGN: Prospective animal study. SETTING: Animal basic science laboratory. SUBJECTS: Male Wistar rats, weighing 250-350 g. INTERVENTIONS: Rats were subjected to cecal ligation and perforation (sepsis group) with saline resuscitation (at 50 mL/kg immediately and 12 hrs after cecal ligation and perforation) or sham operation (control group). MEASUREMENTS AND MAIN RESULTS: Oxidative damage, assessed by the thiobarbituric acid reactive species and the protein carbonyl assays, occurred early (after 6 hrs) in the course of sepsis development in the hippocampus, cerebellum, and cortex. At longer times after sepsis induction (12-96 hrs), there was no evidence of oxidative damage in all analyzed structures. Except for the striatum, earlier in sepsis development (6 hrs) we demonstrated an increase in superoxide dismutase activity without a proportional increase in catalase activity with a consequent increase in the relation of superoxide dismutase/catalase. The balance between these enzymes was restored in the studied structures 12-96 hrs after sepsis induction. CONCLUSIONS: The short-term oxidative damage demonstrated here could participate in the development of central nervous system symptoms during sepsis development, or even septic encephalopathy. The alterations in the superoxide dismutase/catalase relation were temporally related to the occurrence or not of oxidative damage in the central nervous system.