Effects of acute footshock stress on antioxidant enzyme activities in the adolescent rat brain (original) (raw)
Related papers
Neuroscience Letters, 2000
Mild footshock stress results in an increase dopamine metabolism in the prefrontal cortex. Increases in either the intensity or duration of stress enhance dopamine metabolism in the nucleus accumbens and striatum, as well as in the prefrontal cortex. Dopamine is metabolized by monoamine oxidase with hydrogen peroxide as a product. In this study we have demonstrated that while very mild (0.2 mA) footshock stress did not change glutathione peroxidase activity in the rat prefrontal cortex and striatum, more intense (1.6 mA) footshock stress increased glutathione peroxidase activity at 0, 15, 30 and 60 min after the footshock in the prefrontal cortex and at 30 min after the footshock in the striatum. Stress did not change superoxide dismutase activity and thiobarbituric acid reactive substances levels. These results indicate that increased dopamine metabolism induced by footshock stress is probably responsible for the increase of glutathione peroxidase activity.
Antioxidant Enzymes in Brain Cortex of Rats Exposed to Acute, Chronic and Combined Stress
Folia Biologica, 2016
Antioxidant enzymes in brain cortex of rats exposed to acute, chronic and combined stress. Folia Biologica (Kraków) 64: 189-195. The study deals with manganese superoxide dismutase, copper, zinc superoxide dismutase, and catalase activities in brain cortex of Wistar rats exposed to acute stress (immobilization or cold for 2 h), chronic stress (long-term isolation or long-term forced swimming for 21 days), or to combined chronic/acute stress. We observed that i) single episodes of acute stress by immobilization increased activity of both superoxide dismutases; ii) both types of chronic stresses significantly elevated activities of all examined enzymes; iii) chronic social isolation was a much stronger stressor than physical stress by swimming; iv) in animals pre-exposed to chronic isolation, additional stress by immobilization or cold significantly decreased previously elevated activities of all enzymes, while after chronic swimming, acute immobilization lowered only catalase activity. The obtained results indicate that stress conditions most probably altered the cell redox equilibrium, thus influencing the antioxidant response in brain cortex. Further investigation of neuronal prooxidant/antioxidant cellular conditions is needed to improve the prevention and treatment of various stress induced diseases.
Behavioural Brain Research, 2007
The effect of restraint stress (RS) on neurobehavioral and brain oxidative stress parameters, and their modulation by antioxidants were evaluated in male and cycling female rats. Exposure to RS suppressed both open arm entries and open arm time in the elevated plus maze and these changes were more marked in males than in females. Assay of brain homogenates revealed that the behavioral suppression was associated with similar differential increases in malondialdehye (MDA) and decreases in glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) levels in males and females. Pretreatment with ␣-tocopherol (25 and 50 mg/kg) and N-acetylcysteine (100 and 200 mg/kg), attenuated the stress induced alteration of behavioral and oxidative stress markers in a consistent manner in both male and female rats. These findings suggest that males may be more susceptible than females to stress induced neurobehavioral changes and free radicals may exert a regulatory influence in such gender dependent responses to stress.
Journal of Pharmacy Research
The effect of restraint stress (RS) on neurobehavioral and brain oxidative/nitrosative stress markers and their modulation by withaferin A were evaluated in young (2 months) and old (16 months) male Wistar rats. Exposure to RS, induced anxiogenesis when tested in the elevated plus maze (EPM) and open field (OF) tests and such changes were greater in the old as compared to the young rats. These behavioral alterations were associated with enhanced levels of malondialdehyde (MDA) and reductions in glutathione (GSH), catalase (CAT) and nitric oxide metabolites (NOx) levels in brain homogenates-the effects being greater in intensity in the old as compared to the young animals. Pretreatment with withaferin A(20,30,40 and 50 mg/kg) and other antioxidants like alpha-tocopherol (25 and 50 mg/kg) and N-acetylcysteine (100 and 200 mg/kg) consistently reversed the RS-induced behavioral and biochemical alterations in both young and old rats. Withaferin A did inhibit the brain NO synthase activity measured ex vivo by NOx assay. We conclude that a suppression of NO synthase activity may be important in the anxiolyticlike effect of withaferin A in both young and old rats. But old rats are responsive to higher doses of withaferin A as compared to young rats. The results suggest that susceptibility to stress-induced neurobehavioral alterations may increase with age and interactions of reactive oxygen species (ROS) and nitric oxide in the central nervous system may exert a regulatory influence in such age dependent responses to stress.
2000
It has been suggested that oxidative stress is involved in aging and neuropathologic disorders. In addition, chronic stress and high corticosterone levels are suggested to induce neuronal death. The aim of this study is to verify the effect of chronic variate stress on lipoperoxidation and on the total radical-trapping potential (TRAP) in hippocampus, hypothalamus and cerebral cortex. Adult male Wistar rats were submitted to different stressors during 40 days. Lipid peroxide levels were assessed by the thiobarbituric acid reactive species (TBARS) reaction, and TRAP was measured by the decrease in luminescence using the 2-2′-azo-bis(2-amidinopropane)-luminol system. The results showed that in cerebral cortex homogenates chronic stress induces an increase in oxidative stress. In hypothalamus a decreased lipoperoxidation was observed, however TRAP showed no difference. In hippocampus no difference was observed. We concluded that prolonged stress induces oxidative stress which varies selectively with the brain region.
Role of free radicals in stress-induced neurobehavioural changes in rats
2006
Effect of restraint stress (RS) and its modulation by antioxidants were evaluated on elevated plus maze (EPM) and open field (OF) tests in rats. Restraint stress (RS for 1hr) reduced the number of open arm entries, as also the time spent on open arms indicating enhanced anxiogenic response in the EPM test as compared to normal non RS group of rats. Pretreatment with ascorbic acid (100 and 200 mg/kg) and α-tocopherol (30 and 60 mg/kg) attenuated these RS-induced effects. In the OF test, RS-reduced (a) ambulations; and (b) rearings, whereas an increase was seen in (a) latency of entry and (b) number of fecal boluses. The RS-induced changes in OF parameters were reversed after pretreatment with the antioxidants, (ascorbic acid and alpha tocopherol). Biochemical data showed that RS enhanced MDA levels in both serum and brain, and these were attenuated after pretreatment with the antioxidants. The pharmacological and biochemical results indicate that free radicals might be involved in such stress-induced neurobehavioural effects.
Neuropsychiatric Disease and Treatment
Background and Purpose: Ample evidence indicates that chronic adolescence stress is associated with an increased risk of developing neuropsychiatric disorders in adulthood. Given the importance of the effective therapeutic ways to overcome adolescent stress-related deficits, the present study investigated the effects of Spirulina platensis (SP), environmental enrichment (EE), and voluntary exercise (EX) and their combination on anxiety or depression-like behaviors, oxidative stress, and alterations of BDNF and 5HT-3 receptors in the prefrontal cortex (PFC) induced by adolescent stress in adult female rats. Methods: During the adolescent period (PNDs30-40), rats were subjected to restraint stress. Then, the animals were subjected to SP treatment (200 mg/kg/day), EX, EE, and the combined treatments (SP+EX, and SP+EE) for 15 days between PNDs41-55. Subsequently, anxiety or depression-like behaviors, BDNF levels, oxidative stress markers and mRNA expression of BDNF and 5HT 3 in the PFC were assessed. Results: Stressed rats demonstrated enhanced anxiety levels and depression-like behaviors in adulthood. Regarding the oxidative stress markers, stressed rats exhibited significantly higher levels of malondialdehyde, a lipid peroxidation product, higher activities of antioxidant enzymes (glutathione peroxidase and superoxide dismutase) and significantly lower total antioxidant reactivity capacity in the PFC. Additionally, adolescent stress significantly increased 5HT3 receptor mRNA expression and decreased BDNF content and its mRNA expression in the PFC. Treatments with SP, EX, EE, and the combined interventions alleviated these deficits. Conclusion: Our findings indicate that appropriate interventions during the adolescent period can protect against adolescent stress-induced behavioral, and biochemical defects and oxidative stress damage in adulthood.
EXCLI Journal
The aim of this study was to evaluate the effect of acute and chronic physical and psychologi-cal stressors on the induction of oxidative stress in male rat liver. Male Wistar rats were ran-domly divided into 3 groups as following: control, physical and psychological stress groups. Stress was induced by communication box for one (acute), fifteen and thirty (chronic) days. Once stressor periods ended, rats were anesthetized and their liver dissected out for later as-sessments. Exposure to physical stress enhanced liver superoxide dismutase (SOD) (19.44 %) and glutathione S-transferase (GST) (21.84 %) activities and decreased glutathione (GSH) (30.03 %) level on the 1st day (p<0.05). SOD (24.13 and 18.43 %) and GST (27.77 and 21.27 %) activities were significantly increased, while catalase activity (29.74 and 24.41 %) and GSH level (35.05 and 31.05 %) were decreased in psychological stress group after 1 and 15 days (p<0.01 and p<0.05) compared to the 1st day value in control ...
Metabolic Brain Disease, 2010
Since chronic stress has been used widely for studying clinical depression and that brain energy metabolism and oxidative stress might be involved in the pathophysiology of this illness, the objective of this study was investigate the activities of pyruvate kinase, complex II and IV (cytocrome c oxidase) in hippocampus and prefrontal cortex of rats submitted to chronic variable stress. We also evaluated if vitamins E and C administration could prevent such effects. During 40 days adult rats from the stressed group were subjected to one stressor per day, at a different time each day, in order to minimize predictability. The stressed group had gained less weight while its immobilization time in the forced swimming test was greater than that of the control group. Results showed that stressed group presented an inhibition in the activities of complex II and cytochrome c oxidase in prefrontal cortex, while in hippocampus just complex IV was inhibited. Pyruvate kinase activity was not altered in stressed group when compared to control. Vitamins E and C administration prevented the alterations on respiratory chain caused by stress. These data suggest that the impairment of energy metabolism and oxidative stress could be related with the pathogenic pathways in stress related disorders.