scholarly journals Traumatic stress, oxidative stress and post-traumatic stress disorder: neurodegeneration and the accelerated-aging hypothesis

2014 ◽  
Vol 19 (11) ◽  
pp. 1156-1162 ◽  
Author(s):  
M W Miller ◽  
N Sadeh
Keyword(s):  
Oxidative Stress ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Accelerated Aging ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
Stress Oxidative

scholarly journals The Link between Chronic Stress and Accelerated Aging

Biomedicines ◽  
2020 ◽  
Vol 8 (7) ◽  
pp. 198 ◽  
Author(s):  
Yegor E. Yegorov ◽  
Anastasia V. Poznyak ◽  
Nikita G. Nikiforov ◽  
Igor A. Sobenin ◽  
Alexander N. Orekhov
Keyword(s):  
Oxidative Stress ◽  
Chronic Stress ◽  
Traumatic Stress ◽  
Accelerated Aging ◽  
Post Traumatic Stress ◽  
Mitochondrial Uncoupling ◽  
Post Traumatic ◽  
Stress Oxidative ◽  
Inflammatory Changes ◽  
Component Gene

People exposed to chronic stress age rapidly. The telomeres in their cells of all types shorten faster. Inflammation is another important feature of stress that, along with aging, accounts for the phenomenon of inflammaging. In addition to aging itself, inflammaging can contribute to the development of several pathologies, including atherosclerosis, diabetes, hypertension, and others. Oxidative stress is one of the main mechanisms related to stress. Oxidative stress is caused by the over-production of reactive oxygen species (ROS) that can damage various tissues. The main source of ROS is mitochondria. Being suppressed by mitochondrial mutations, mitophagy can aggravate the situation. In this case, the aging-specific pro-inflammatory changes are amplified. It happens because of the inability of cells to maintain the normal state of mitochondria. Macrophages are the crucial element of the innate immunity associated with the chronic inflammation and, subsequently, with the inflammaging. In this review, we focus on the therapy approaches potentially reducing the deleterious effects of oxidative stress. These include stimulation of mitophagy, activation of mitochondrial uncoupling, induction of the expression of the telomerase catalytic component gene, and use of antioxidants. Any method reducing oxidative stress should improve post-traumatic stress disorder.

Serum total oxidant and antioxidant status in earthquake survivors with post-traumatic stress disorder

2015 ◽  
Vol 27 (3) ◽  
pp. 153-158 ◽  
Author(s):  
Pinar Guzel Ozdemir ◽  
İbrahim Kaplan ◽  
Cem Uysal ◽  
Mahmut Bulut ◽  
Abdullah Atli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Antioxidant Status ◽  
Stress Disorder ◽  
Total Antioxidant Status ◽  
Post Traumatic Stress ◽  
Total Antioxidant ◽  
Post Traumatic ◽  
Earthquake Survivors

ObjectiveOxidative stress has been shown to play an important role in the pathogenesis of post-traumatic stress disorder (PTSD). Although there are some studies on oxidative stress and PTSD, there is no report available on the serum total oxidant and antioxidant status in earthquake survivors with PTSD. Therefore, this study aimed to investigate the serum total oxidant and antioxidant status in earthquake survivors with chronic PTSD.Material and MethodsThe study group included 45 earthquake survivors with PTSD and 40 earthquake survivors without PTSD. The oxidative status was determined using the total antioxidant status and total oxidant status (TOS) measurements and by calculating the oxidative stress index (OSI).ResultsThere were no statistically significant differences in the total antioxidant status, TOS, or OSI when comparing individuals with and without PTSD (all,p>0.05). There were no correlations between Clinician-Administered PTSD Scale scores and oxidant and antioxidant stress markers (all,p>0.05).ConclusionsOur results suggest that the total oxidant and antioxidant status may not affect earthquake survivors with PTSD. This is the first study to evaluate the oxidative status in earthquake survivors with PTSD. Further studies are necessary to confirm these findings.

L-Carnitine prevents memory impairment induced by post-traumatic stress disorder

2021 ◽  
pp. 1-9
Author(s):  
Karem H. Alzoubi ◽  
Arwa M. Al-Dekah ◽  
Saied Jaradat ◽  
Nasr Alrabadi
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Memory Impairment ◽  
Stress Disorder ◽  
Post Traumatic Stress ◽  
Short And Long Term ◽  
Post Traumatic

Background: Post-traumatic stress disorder (PTSD) is a genuine obstructing mental disorder. As indicated by the name, it is related to the patients’ stress augmented by life-threatening conditions or accidents. The PTSD has linked to oxidative stress that can result in neurodegeneration. L-carnitine (L-CAR) is known for its antioxidant properties, which can protect against neuronal damage. Objective: In the current study, we investigated the beneficial effects of L-CAR on the memory impairment induced by PTSD using a rat model. Methods: A model of single-prolonged stress (a cycle of restraining, forced swimming, rest, and finally diethyl ether exposure for 2 h, 20 min, 15 min, and 1–2 min, respectively) was used to induce PTSD-like behavior. Intraperitoneal L-CAR treatment (300 mg/kg/day) was introduced for four weeks. Both memory and special learning were evaluated utilizing the radial arm water maze (RAWM). Moreover, the levels of glutathione peroxidase (GPx), glutathione reduced (GSH), and glutathione oxidized (GSSG) were assessed as biomarkers oxidative stress in the hippocampus. Results: The results demonstrated that both the short and long-term memories were impaired by PTSD/SPS model (P <  0.05), while L-CAR treatment prevented this memory impairment in PTSD rats. Besides, L-CAR prevented the reduction in GPx activity and increase in GSSG, which were altered in the hippocampus of the PTSD/SPS rats (P <  0.05). Levels of GSH were not changed in PTSD and/or L-CAR rats. Conclusions: L-CAR administration prevented short- and long-term memories’ impairments induced in the PTSD/SPS rat model. This is probably related to its antioxidant effects in the hippocampus.

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