scholarly journals Low-dose irradiation reduces forced swim test-induced immobility and oxidative stress in mice

2021 ◽  
Vol 165 ◽  
pp. 56-57
Author(s):  
Shota Naoe ◽  
Takahiro Kataoka ◽  
Hina Shuto ◽  
Junki Yano ◽  
Tetsuya Nakada ◽  
...  
2020 ◽  
Vol 61 (4) ◽  
pp. 517-523
Author(s):  
Takahiro Kataoka ◽  
Hina Shuto ◽  
Junki Yano ◽  
Shota Naoe ◽  
Tsuyoshi Ishida ◽  
...  

Abstract The forced swim test (FST) is a screening model for antidepressant activity; it causes immobility and induces oxidative stress. We previously reported that radon inhalation has antidepressant-like effects in mice potentially through the activation of antioxidative functions upon radon inhalation. This study aimed to investigate the effect of prior and post low-dose X-irradiation (0.1, 0.5, 1.0 and 2.0 Gy) on FST-induced immobility and oxidative stress in the mouse brain, and the differences, if any, between the two. Mice received X-irradiation before or after the FST repeatedly for 5 days. In the post-FST-irradiated group, an additional FST was conducted 4 h after the last irradiation. Consequently, animals receiving prior X-irradiation (0.1 Gy) had better mobility outcomes than sham-irradiated mice; however, their levels of lipid peroxide (LPO), an oxidative stress marker, remained unchanged. However, animals that received post-FST X-irradiation (0.5 Gy) had better mobility outcomes and their LPO levels were significantly lower than those of the sham-irradiated mice. The present results indicate that 0.5 Gy X-irradiation after FST inhibits FST-induced immobility and oxidative stress in mice.


2019 ◽  
Vol 70 (11) ◽  
pp. 4102-4104

With magnesium being an essential element in the human body, we are proposing here an original study on the correlations between magnesium and depression and their cardiovascular relevance in this context, by the usage of the experimental forced swim test. Thus, the data we are presented here could have an increased relevance in the management of these disorders, and in the further understanding of the biochemical magnesium supplementation. Keywords: magnesium, depression, oxidative stress, cardiovascular


2010 ◽  
Vol 25 (2) ◽  
pp. 125-133 ◽  
Author(s):  
Mmalebuso L. Mokoena ◽  
Brian H. Harvey ◽  
Douglas W. Oliver ◽  
Christiaan B. Brink

2020 ◽  
Vol 71 (6) ◽  
pp. 247-253
Author(s):  
Roxana-Rosmary Enciu ◽  
Constantin Trus ◽  
Sorin Ungurianu

Aspartame is a worldwide used artificial sweetener and is consumed by millions of adults and children as part of their diet. The connection between aspartame ingestion and depression has been studied with contradictory results. We hypothesized that this correlation might be explained by high levels of oxidative stress. We wanted to examine the biochemical effects of consuming higher or lower doses of aspartame on the antioxidant enzyme- glutathione peroxidase (GPX) and on the depression-like behaviors of rats in the forced swim test model. 40 lab rats were divided into 4 groups; two groups were treated by gavage with either 75 mg/kg/day of aspartame or 125 mg/kg/day of aspartame. The control group received a gavage with vehicle (water). The naive group received no experimental intervention. Our statistical analysis revealed that the rats from the control group and the naive group presented a significantly lower level of GPX compared to the groups that received 75mg/kg/day or the group that received the maximum dosage of 125mg/kg/day aspartame. Furthermore, a shorter duration of the immobility was reported in the control and the naive groups when compared to the groups which received any of the two dosages of aspartame. Therefore, the results presented by our study suggest that aspartame consumption (in both high and low dosages) increases both the oxidative stress and the depression-like symptoms in the forced swim model. In addition, an aspartame dose-response was not found for either of our two variables: oxidative stress or depression. In conclusion, the daily consumption of aspartame for 4 weeks, in both high dosage and low dosage, had a negative impact on both oxidative stress level and the frequency of depression- like behaviors of the animals in the forced swim test. These results suggest that the correlation between aspartame ingestion and depression might be explained by oxidative stress levels.


2020 ◽  
Vol 16 (9) ◽  
pp. 1319-1327
Author(s):  
Ferdous Khan ◽  
Syed A. Kuddus ◽  
Md. H. Shohag ◽  
Hasan M. Reza ◽  
Murad Hossain

Background: An imbalance between pro-oxidants and antioxidants determines the level of oxidative stress which is implicated in the etiopathogenesis of various neuropsychiatric disorders including depression. Therefore, treatment with antioxidants could potentially improve the balance between pro-oxidants and antioxidants. Objective: The objective of this study was to evaluate the ability of astaxanthin, a potential antioxidant, to reduce reserpine-induced depression in BALB/c mice (Mus musculus). Methods: On the behavioral level, antidepressant property of astaxanthin (50 mg/kg, orally) on reserpine (2 mg/kg, subcutaneously) induced depressed mice was evaluated by Forced Swim Test (FST) and Tail Suspension Test (TST). In the biochemical level, the ability of astaxanthin to mitigate reserpine-induced oxidative stress was evaluated by the measurement of Malondialdehyde (MDA) and nitric oxide (NO) in brain, liver and plasma samples. On the other hand, the efficiency of astaxanthin to replenish glutathione depletion and antioxidant enzyme activity augmentation in the same samples were also investigated. Results: Astaxanthin was able to lower reserpine induced immobility time significantly (p<0.05) in FST and TST. Mice treated with astaxanthin showed significantly (p<0.05) low level of oxidative stress markers such as Malondialdehyde (MDA), Nitric Oxide (NO). Consistently, the level of reduced Glutathione (GSH), and the activity of Superoxide Dismutase (SOD) and catalase were augmented due to the oral administration of astaxanthin. Conclusion: This study suggests that astaxanthin reduces reserpine-induced oxidative stress and therefore might be effective in treating oxidative stress associated depression.


Author(s):  
Roni Yankelevitch-Yahav ◽  
Motty Franko ◽  
Avrham Huly ◽  
Ravid Doron

2019 ◽  
Vol 236 (11) ◽  
pp. 3353-3362 ◽  
Author(s):  
Mohammad Nasehi ◽  
Mohammad-Hossein Mohammadi-Mahdiabadi-Hasani ◽  
Mohaddeseh Ebrahimi-Ghiri ◽  
Mohammad-Reza Zarrindast

2021 ◽  
pp. 1-7
Author(s):  
Dylan J. Terstege ◽  
Debra S. MacDonald ◽  
R. Andrew Tasker

Abstract Objective: Ginsenosides, biologically active components of the root of Panax ginseng, have been reported to have therapeutic benefits in a number of disease states including psychiatric conditions such as major depressive disorder. Our objective was to determine if a standardised commercial ginseng extract, G115®, could reduce the signs of behavioural despair commonly observed in animal models of depression either alone or in combination with the selective serotonin reuptake inhibitor (SSRI) fluoxetine. Methods: Male Sprague-Dawley (SD) rats (N = 51) were divided into four groups: vehicle control, G115® ginseng root extract, fluoxetine and fluoxetine plus G115®. Rats were trained to voluntarily consume treatments twice daily for 14 days and were then tested in an open field (OF), elevated plus maze (EPM) and forced swim test (FST). Post-mortem hippocampal and prefrontal cortex tissue was analysed for expression of brain-derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) by western blot. Results: One-way Analysis of Variance revealed no significant group differences in the OF or plus-maze performance on any variable examined. In the FST, fluoxetine significantly reduced immobility time and increased latency to immobility. The effects of fluoxetine were further significantly potentiated by co-administration of G115®. Post-mortem tissue analysis revealed significant group differences in BDNF expression in the left hippocampus and left prefrontal cortex without any accompanying changes in TrkB expression. Conclusions: We conclude that oral G115® significantly potentiates the antidepressant-like effect of fluoxetine in the FST in the absence of potentially confounding effects on locomotion and anxiety.


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