Antioxidant Enzyme Activities In Brain Research Articles

Unpredictable chronic mild stress induced anxio-depressive disorders and enterobacteria dysbiosis: Potential protective effects of Detariummicrocarpum

Ethnopharmacological relevanceDetarium microcarpum Guill. & Perr. is used traditionally in Far North Cameroun to treat stomach aches, anxiety, epilepsy, and other mental disorders. Aim of the studyEvaluate the anxiolytic and antidepressant-like effects of D. microcarpum (DM) in unpredictable chronic mild stress (UCMS) model of depression in male rats and its impact on fecal enterobacteria of stressed rats. Materials and methodsRats were handled daily (control) or subjected to the UCMS procedure for 42 days. Anxiety-like behaviors were assessed using the light and dark box test (LBD) and the open field test (OFT). Depressive-like behaviors were assessed using the forced swimming test (FST), the sucrose preference test (SPT), and the novelty suppressed feeding test (NSFT). Feces were then collected, followed by blood, brain, and duodenum sections after sacrifice. Monoamine levels, pro-inflammatory cytokines, oxidative stress factors, and nitrosative stress were assessed. Feces were introduced into Hectoen enteric agar for the identification of enterobacteria. An in vitro growth test was performed. ResultsThe DM ethanolic extract has significantly increased the time spent in the light box, in the LBD, and in the center area of the OFT. Moreover, the extract has significantly reduced the preference for sucrose in the SPT, the time of immobility in the FST, and the latency period to consume the pet in the NSFT. DM extract has significantly reduced serum cortisol levels. It also significantly decreased the pro-inflammatory cytokines TNF-α and Il-1β in both brain and duodenum homogenate. DM has increased the brain's serotonin, GABA, and dopamine levels. The DM extract also decreased the MDA and nitrite levels. It also increased the SOD and CAT activities in both brain and duodenal homogenate. Histologically, the DM extract restored the cell's density in hippocampi sections and prevented gut inflammation and peroxidation characterizing leaky gut syndrome. DM extract has no effect on the growth of enterobacteria species isolated in vitro. ConclusionThe ethanolic extract of DM would have anxiolytic and antidepressant effects via the modulation of the HPA axis, brain antioxidant enzyme activities, inflammation, and nitrosative stress. Moreover, it could act by preventing leaky gut syndrome.

Neuroprotective potential of Argan oil in neuropsychiatric disorders in rats: A review

• AO exhibit a neuroprotection against certain aspects of neuropsychiatric disorders. • AO neuroprotection may be due to synergistic effects of its bioactive compounds. • AO modulates the brain antioxidant enzyme activities and the anti-inflammatory system. • AO can regulate the HPA axis activities, neurotransmitter pathways and the brain neuroplasticity processes. Argan Oil (AO), a natural vegetable oil, commonly used in folk Moroccan medicines. Preclinical studies, uphold that AO may exhibit neuroprotection against several aspects of neuropsychiatric disorders such as addiction, depression and epilepsy. This paper attempts to collate those experimental findings. Moreover, the benefits of AO in vitro on nerve cells is pointed out. AO is principally composed of mono- unsaturated and saturated fatty acids. As minor components, it contains polyphenols, tocopherols and sterols, among other. The reason for AO's obvious neuroprotective effects in this review may be due to synergistic effects of these bioactive compounds which are especially effective on central nervous system. We suggest that these effects can be the result of modulation of brain antioxidant enzyme and anti-inflammatory system, as well as by the possible regulation of the stress axis and the brain neuroplasticity processes. Further studies are needed to fully characterize AO from neuro-pharmacological and nutritional perspectives.

Syzygium malaccense fruit supplementation protects mice brain against high-fat diet impairment and improves cognitive functions

Abstract In this study, we supplemented a high-fat diet (HF) with 5% powder of freeze-dried Syzygium malaccense fruit (HS) and investigated proofs of peripheral insulin resistance, hippocampal AKT–GSK3-β–tau activation, learning/memory performance, and brain frontal lobe oxidative stress. The intake of HS did not prevent weight gain but promoted peripheral insulin sensitivity, improved AKT signaling in the hippocampus, which prevented the activation of GSK3-β and lowered tau phosphorylation induced in HF. The results from the Morris water maze cognitive test were consistent with the lower tau-phosphorylation, once the HS group showed lower latency in the acquisition phase and more times crossing the target quadrant when compared with HF. The HS diet improved brain antioxidant enzyme activities. Overall, the intervention with S. malaccense fruit to mice was effective in minimizing cognitive deficit caused by HF consumption and in preventing risk markers associated with Alzheimer’s disease without reducing weight gain in mice.

Anti-Obesity Effects of Tocotrienols and Bran in High-Fat Diet-Treated Mice.

Obesity is a serious public health issue in developed countries, and is known to increase the risk of several diseases such as diabetes, cardiovascular events and arteriosclerosis. These phenomena are closely correlated with oxidative damage. Recently, several lines of evidence have demonstrated that neurodegenerative diseases such as Alzheimer’s and Parkinson’s are also related to oxidative damage. To clarify the relationship between obesity and oxidative brain injury, we investigated brain antioxidant networks in high-fat (HF) diet-treated mice in the presence or absence of tocotrienols (T3s) and bran. Co-treatment with T3s and bran significantly inhibited bodyweight gain in HF diet-treated mice. Serum and cortex T3 levels, and brain antioxidant enzyme activities and protein expressions did not differ among the groups except for SOD protein expression in the cerebellum. Brain p-mTOR and p-Akt protein expressions, which are related to autophagy, did not differ among the groups. These results indicate that treatment with T3s for eight weeks had showed an anti-obesity effect in HF diet-treated mice. However, significant alterations in T3 levels were not observed in the serum and brain of mice.

Argan Oil Supplementation Reverses Anxiety and Depressive-Like Behaviors, Neurodegeneration and Oxidative Stress in Amygdala Induced by Chronic Mild Stress in Rats

Background: Argan Oil (AO) has been used as a natural remedy in traditional medicine, mainly in Morocco, for several centuries. In this study, we evaluated the beneficial effects of AO dietary on vulnerability of rats to the chronic unpredictable mild stress (UCMS) using behavioral tests, biochemical and histological markers of depression or anxiety. Method: Rats were handled daily (home cage control) or subjected to the UCMS procedure during 6 weeks (i.e., from 43th to 85 Post-natal Day (PND)) (Stress group, n=12). Animals were previously administered orally by NaCl 0.9% (Control group, n=11) or AO (10 ml/kg/day) (AO+Stress group, n=12) for 10 weeks (i.e., from weaning 21th to 93 PND). The efficacy of UCMS or AO dietary on behavioral performances of the animals in the open field, the forced swimming, the light/dark, the novelty suppression of feeding and sucrose preference tests, was measured. Following behavioral assays, oxidative stress in amygdala, histologic semiquantitative analysis of neurodegeneration in the hippocampus, frontal cortex and basolateral amygdala (BLA) subregions, and corticosterone level in plasma was also performed. Results: Our data supports pharmacological and biochemical evidences for the antidepressant and anxiolytic-like effects of AO. Prolonged supplementation with AO reverses all the behavioral changes that occurred due to UCMS and restored corticosterone level in the plasma, oxidative status of amygdala and the neurons level in the CA3 subregion of rats’ hippocampus. Conclusion: This study suggests that antidepressant and anxiolytic like effects of AO in adult rats can be the result of modulation of brain antioxidant enzyme activities, the activation of hippocampal neurogenesis and the modulation of HPA axis activity. However, more experiment and detailed analysis is required for definitive conclusion.

Microsomal Lipid Peroxidation, Antioxidant Enzyme Activities in Brain of Male Rats during Long-Term Exposure to Isoniazid

Isoniazid, a broad-spectrum antibiotic employed clinically in the treatment of bacterial infections, is known to cause a number of biochemical dysfunctions and suspected to induce memory decline with age to animals and humans. The present study therefore evaluates the oxidative damage in brain albino male rats. Isoniazid was administered orally at the dose regimen level of 5.0 mg/kg body weight per day in three equal divided doses of 10, 20, 30mg/kg (12 h interval) for 60 days. Control rats were given distilled water for the same period. Administration of Isoniazid significantly decreased the activity of superoxide dismutase. The activity of gamma-glutamyltranspeptidase, the activity of alanine-amino transferase (ALT) and alkaline phosphatase (ALP) as well as the formation of malondialdehyde (MDA) increased (p<0.05) compared to the corresponding control. The toxic effects of Isoniazid to the brain antioxidant defence systems were significantly increased. Collectively, the results suggest that therapeutic dose of Isoniazid elicits brain lesions in male rats through induction of oxidative damage and via the inhibitory effect on protein synthesis.

Effects of structural analogues of nociceptin(1–13)NH2 on brain antioxidant status in kainic acid‐treated rats

The in vivo effects of nociceptin (N/OFQ(1-13)NH(2) ) and its structural analogues ([Dab(9) ]N/OFQ(1-13)NH(2) , [Dap(9) ]N/OFQ(1-13)NH(2) and [Cav(9) ]N/OFQ(1-13)NH(2) ) on the levels of lipid peroxidation and cell antioxidants (enzyme and non-enzyme) in brain of control and kainic acid (KA)-treated rats were studied. In control animals, [Dab(9) ]N/OFQ(1-13)NH(2) and [Dap(9) ]N/OFQ(1-13)NH(2) , unlike N/OFQ(1-13)NH(2) and [Cav(9) ]N/OFQ(1-13)NH(2) , slightly increased the brain lipid peroxidation; the rest of the parameters were unchanged by all neuropeptides tested. KA (0.25 µg in 0.5 µl, i.c.v) increased the lipid peroxidation (4 and 24 h after KA-injection) and decreased the glutathione level (1 h after KA-administration). One hour after KA-administration, the neuropeptides (2 µg in 0.5 µl, injected 30 min before KA) showed the following effects: a slight decrease in the KA-induced lipid peroxidation by all nociceptin analogues and an enhancement of the KA-decreased GSH level, but by [Cav(9) ]N/OFQ(1-13)NH(2) only. The brain antioxidant enzyme activities were unchanged in all used experimental groups. In addition, the nociceptin analogues, especially [Can(9) ]N/OFQ(1-13)NH(2) , showed a good antioxidant capacity in chemical systems, generating reactive oxygen species. In conclusion, the substitution of lysin (Lys) in N/OFQ(1-13)NH(2) molecule with other amino acids might contribute to changes in its antioxidant properties. Copyright © 2011 John Wiley & Sons, Ltd.

Phase II antioxidant enzyme activities in brain of male and female ACI rats treated chronically with estradiol

Activities of Phase II antioxidant enzymes, including NAD(P)H:quinone oxidoreductase 1 (NQO1), glutathione S-transferase (GST), UDP-glucuronosyltransferase (UGT), and phenol sulfotransferase 1A1 (SULT1A1) were measured in brain of August–Copenhagen Irish (ACI) rats exposed chronically to low doses of estradiol (E 2). ACI rats were selected for study because this strain is highly responsive to treatment with low doses of E 2 as indexed by a high incidence of E 2-induced mammary tumors compared to other strains. Rats were exposed chronically to 3 mg E 2 contained in cholesterol pellets implanted subcutaneously for 6 weeks. This treatment increased activities of all four enzymes in the striatum of male but not female ACI rats. Blood E 2 levels at time of sacrifice correlated closely with activities of striatal NQO1, GST, and SULT1A1, but not with striatal UGT. NQO1, GST, and SULT1A1 activities in other brain regions including the cortex, cerebellum, and hippocampus were less sensitive to chronic E 2 treatment. NQO1 was primarily localized in vascular elements and neurons and SULT1A1 primarily in neurons and neuropil of control and E 2-treated rats. Collectively, these results suggest that enhanced expression of NQO1, GST, and SULT1A1 may contribute to the antioxidant effects of E 2 in the striatum, an area of the brain that may be particularly prone to oxidative stress because of its high content of catecholamines.

Positive effects of deprenyl and estradiol on spatial memory and oxidant stress in aged female rat brains

Increasing age decreases spatial learning and memory. Spatial learning is coordinated with different brain regions. Since the oxidative damage may play a role in the aging process, including the associated cognitive decline, age-related impairment in spatial learning and memory may be alleviated by antioxidant treatment. The present study examined the effects of the monoamine oxidase B inhibitor l-deprenyl, alone and in combination with estradiol, on spatial memory using the Morris water maze and oxidant stress in aged female rat brains. We demonstrated that co-administration of deprenyl and estradiol caused a synergistic effect on spatial memory. However, use of either deprenyl or estradiol alone increased antioxidant enzyme activities in brain and reduced lipid peroxidation. Therefore, positive effects of deprenyl and estradiol on spatial memory may occur due not only to their antioxidant activities but also to the different actions.

Basal and drug-induced antioxidant enzyme activities correlate with age-dependent doxorubicin oxidative toxicity

Doxorubicin continues to be one of the most widely used anticancer agents in the clinic despite its dose-limiting side-effects. Many of doxorubicin’s dose-limiting toxicities occur due to its generation of toxic oxygen species, resulting in oxidative stress. Some clinical observations have suggested that doxorubicin may have greater toxicity in older patients. The studies presented here compare basal and doxorubicin-induced antioxidant enzyme activities in brain, heart, kidney and liver tissues of Fisher 344 rats of different ages to determine whether differences in these enzymes can account for the age-dependent differences observed in doxorubicin-induced toxicity. Three groups of animals were tested, young animals (2-months-old), adult animals (10-months-old) and old animals (18-months-old). The results of these studies show that in general young and adult animals have similar levels of antioxidant enzyme activity while the older animals have less. Only in the young animals is antioxidant enzyme activity significantly increased following doxorubicin treatment suggesting that enzyme induction occurs only in the young group of animals. Lipid peroxidation is shown to have the greatest increase in the old animals following doxorubicin treatment while the young animals have the smallest increase. The results from these studies suggest that there is an increase in doxorubicin-induced oxidative damage with age and that these differences may be due to basal and drug-induced differences in tissue antioxidant enzyme activities.

Electroconvulsive shock in rats: changes in superoxide dismutase and glutathione peroxidase activity

Seizures trigger a variety of biochemical processes including an influx of extracellular Ca 2+, activation of membrane phospholipases, liberation of free fatty acids, diacylglycerols, eicosanoids, lipid peroxides and free radicals. These lipid metabolites along with abnormal ion homeostasis may be involved in cell injury and cell death. The aim of this study was to determine brain antioxidant enzyme activities in rats with electroconvulsive shock (ECS)-induced seizures. ECS, single or repeated, induced a decrease in superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities in various brain regions. The most prominent changes of enzymatic activities were observed in rats that received five ECSs with 24-h recovery period between them. Decreased SOD activity was observed in the frontal cortex of all treated animals except those sacrificed 24 h after single ECS, in the cerebellum of the animals that received repeated ECSs, in the hippocampus of animals that were decapitated 2 h after a single ECS and in the pons–medulla region of rats that received five daily ECSs. Decreased GPX activity was found in all examined brain regions of the rats that received five ECSs, the cortex and hippocampus of rats that were decapitated 2 h after single ECS and the cortex of those that received 10 ECSs with 48 h between them. The results show that neither 24-h nor 48-h recovery period was sufficient for the normalisation of antioxidative enzyme activities after repeated ECS treatment.