Long term treadmill exercise affects age-related oxidative stress in the spinal cord of rats

2020 ◽  
pp. 1-8
Author(s):  
G. Shokouhi ◽  
N. Ahmadiasl ◽  
L. Roshangar ◽  
A. Ghorbanihaghjo ◽  
F. Sheikhzadeh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Treadmill Exercise ◽  
Male Rats ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Groups ◽  
Antioxidant Defence ◽  
Age Related ◽  
Induced Apoptosis

Age-induced apoptosis is believed to be caused by the imbalance between production of reactive oxygen species (ROS) and human body antioxidant defence. Regular aerobic treadmill-exercise has been suggested to enhance the antioxidant defence. This study aimed to investigate the effects of long-term treadmill exercise on age-related oxidative stress and the apoptosis of oligodendrocytes in the spinal cord of the rat. Sixty male rats were divided into six groups: three exercised groups, which underwent 6, 9 and 12 months of mild-to-moderate treadmill exercise and three non-exercised control groups. Spinal cord white or grey matter tissue sampling was done through mid-thoracic laminectomy. The malondialdehyde (MDA; indicator of oxidative stress) levels, the number of apoptotic oligodendrocytes and ultrastructural alterations were also evaluated. Our data showed that treadmill exercise resulted in decreased lipid peroxidation and the number of apoptotic oligodendrocytes in the spinal cord of rats, as compared to non-exercised animals. These results were confirmed by TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labelling) staining and electron microscope. This study suggests that the long-term treadmill exercise can affect oxidative stress and oligodendrocytes apoptosis in the spinal cord of aged rats and further studies are needed to validate these findings in humans.

scholarly journals Crosstalk between Long-Term Sublethal Oxidative Stress and Detrimental Inflammation as Potential Drivers for Age-Related Retinal Degeneration

Antioxidants ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 25
Author(s):  
Lara Macchioni ◽  
Davide Chiasserini ◽  
Letizia Mezzasoma ◽  
Magdalena Davidescu ◽  
Pier Luigi Orvietani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Age Related Macular Degeneration ◽  
Inflammasome Activation ◽  
Related Factor ◽  
Nuclear Factor ◽  
Rpe Cells ◽  
Age Related ◽  
Oxidative Insult

Age-related retinal degenerations, including age-related macular degeneration (AMD), are caused by the loss of retinal pigmented epithelial (RPE) cells and photoreceptors. The pathogenesis of AMD, deeply linked to the aging process, also involves oxidative stress and inflammatory responses. However, the molecular mechanisms contributing to the shift from healthy aging to AMD are still poorly understood. Since RPE cells in the retina are chronically exposed to a pro-oxidant microenvironment throughout life, we simulated in vivo conditions by growing ARPE-19 cells in the presence of 10 μM H2O2 for several passages. This long-term oxidative insult induced senescence in ARPE-19 cells without affecting cell proliferation. Global proteomic analysis revealed a dysregulated expression in proteins involved in antioxidant response, mitochondrial homeostasis, and extracellular matrix organization. The analyses of mitochondrial functionality showed increased mitochondrial biogenesis and ATP generation and improved response to oxidative stress. The latter, however, was linked to nuclear factor-κB (NF-κB) rather than nuclear factor erythroid 2–related factor 2 (Nrf2) activation. NF-κB hyperactivation also resulted in increased pro-inflammatory cytokines expression and inflammasome activation. Moreover, in response to additional pro-inflammatory insults, senescent ARPE-19 cells underwent an exaggerated inflammatory reaction. Our results indicate senescence as an important link between chronic oxidative insult and detrimental chronic inflammation, with possible future repercussions for therapeutic interventions.

scholarly journals Age-related cognitive impairment is associated with long-term neuroinflammation and oxidative stress in a mouse model of episodic systemic inflammation

2018 ◽  
Vol 15 (1) ◽  
Author(s):  
Joana Costa d’Avila ◽  
Luciana Domett Siqueira ◽  
Aurélien Mazeraud ◽  
Estefania Pereira Azevedo ◽  
Debora Foguel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Mouse Model ◽  
Systemic Inflammation ◽  
Age Related ◽  
And Oxidative Stress

scholarly journals Age-related increase of oxidative stress-induced apoptosis in micePrevention by Ginkgo biloba extract (EGb761)

2001 ◽  
Vol 108 (8) ◽  
pp. 969-978 ◽  
Author(s):  
K. Schindowski ◽  
S. Leutner ◽  
S. Kressmann ◽  
A. Eckert ◽  
W. E. Müller
Keyword(s):  
Oxidative Stress ◽  
Ginkgo Biloba ◽  
Ginkgo Biloba Extract ◽  
Age Related ◽  
Induced Apoptosis ◽  
Related Increase

scholarly journals CRISPR/dCas9-Mediated Parkin Inhibition Impairs Mitophagy and Aggravates Apoptosis of Rat Nucleus Pulposus Cells Under Oxidative Stress

2021 ◽  
Vol 8 ◽  
Author(s):  
Tao Lan ◽  
Yu-chen Zheng ◽  
Ning-dao Li ◽  
Xiao-sheng Chen ◽  
Zhe Shen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nucleus Pulposus ◽  
Pathological Condition ◽  
Protective Role ◽  
Intervertebral Disk ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Regulation Mechanism ◽  
Nucleus Pulposus Cells ◽  
Induced Apoptosis ◽  
Design And Methods

ObjectiveThe aim of this study is to explore the role of Parkin in intervertebral disk degeneration (IDD) and its mitophagy regulation mechanism.Study design and methodsRat nucleus pulposus (NP) cells were stimulated with hydrogen peroxide (H2O2) to a mimic pathological condition. Apoptosis and mitophagy were assessed by Western blot, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and immunofluorescence staining. The CRISPR–dCas9–KRAB system was used to silence the expression of Parkin.ResultIn this study, we found that Parkin was downregulated in rat NP cells under oxidative stress. In addition, treatment with H2O2 resulted in mitochondrial dysfunction, autophagy inhibition, and a significant increase in the rate of apoptosis of NP cells. Meanwhile, mitophagy inhibition enhanced H2O2-induced apoptosis. Furthermore, repression of Parkin significantly attenuated mitophagy and exacerbated apoptosis.ConclusionThese results suggested that Parkin may play a protective role in alleviating the apoptosis of NP cells via mitophagy, and that targeting Parkin may provide a promising therapeutic strategy for the prevention of IDD.

Di(2-ethylhexyl)phthalate induces reproductive toxicity via JAZF1/TR4 pathway and oxidative stress in pubertal male rats

2019 ◽  
Vol 35 (3) ◽  
pp. 228-238 ◽  
Author(s):  
Yu-Qin Shi ◽  
Guo-Qing Fu ◽  
Jing Zhao ◽  
Shen-Zhou Cheng ◽  
You Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Morphological Changes ◽  
Reproductive Toxicity ◽  
Male Reproduction ◽  
Male Rats ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Cyclin A1 ◽  
Ethylhexyl Phthalate ◽  
Dehp Exposure ◽  
And Oxidative Stress

Di(2-ethylhexyl)phthalate (DEHP) is a typical endocrine-disrupting chemical and reproductive toxicant. Although previous studies have attempted to describe the mechanism by which DEHP exposure results in reproductive dysfunction, few studies focused on puberty, a critical period of reproductive development, and the increased susceptibility to injury in adolescents. To elucidate the mechanism underpinning the testicular effects of DEHP in puberty, we sought to investigate the JAZF1/TR4 pathway in the testes of pubertal rats. Specifically, we focused on the role of the JAZF1/TR4 pathway in male reproduction, including the genes JAZF1, TR4, Sperm 1, and Cyclin A1. In the present study, rats were exposed to increasing concentrations of DEHP (0, 250, 500, and 1000 mg/kg/day) by oral gavages for 30 days. Then we assayed testicular zinc and oxidative stress levels. Our results indicated that DEHP exposure could lead to oxidative stress and decrease the contents of testicular zinc. Additionally, significant morphological changes and cell apoptosis were observed in testes exposed to DEHP, as identified by hematoxylin and eosin staining and the terminal deoxynucleotidyl transferase-mediated nick and labeling assay. By measuring the expression levels of the above relevant genes by qPCR, we found the DEHP-induced increased expression of JAZF1 and decreased expression of TR4, Sperm 1, and Cyclin A1. Therefore, we have demonstrated that in vivo exposure to DEHP might induce reproductive toxicity in pubertal male rats through the JAZF1/TR4 pathway and oxidative stress.

Long-Term Dietary Extra-Virgin Olive Oil Rich in Polyphenols Reverses Age-Related Dysfunctions in Motor Coordination and Contextual Memory in Mice: Role of Oxidative Stress

2012 ◽  
Vol 15 (6) ◽  
pp. 601-612 ◽  
Author(s):  
Vanessa Pitozzi ◽  
Michela Jacomelli ◽  
Dolores Catelan ◽  
Maurizio Servili ◽  
Agnese Taticchi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Olive Oil ◽  
Motor Coordination ◽  
Virgin Olive Oil ◽  
Extra Virgin Olive Oil ◽  
Contextual Memory ◽  
Age Related

scholarly journals Long-Term Adverse Effects of Oxidative Stress on Rat Epididymis and Spermatozoa

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 170 ◽  
Author(s):  
Pei You Wu ◽  
Eleonora Scarlata ◽  
Cristian O’Flaherty
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Sperm Quality ◽  
Dna Oxidation ◽  
Male Rats ◽  
Saline Control ◽  
Control Group ◽  
Long Term Effects

Oxidative stress is a common culprit of several conditions associated with male fertility. High levels of reactive oxygen species (ROS) promote impairment of sperm quality mainly by decreasing motility and increasing the levels of DNA oxidation. Oxidative stress is a common feature of environmental pollutants, chemotherapy and other chemicals, smoke, toxins, radiation, and diseases that can have negative effects on fertility. Peroxiredoxins (PRDXs) are antioxidant enzymes associated with the protection of mammalian spermatozoa against oxidative stress and the regulation of sperm viability and capacitation. In the present study, we aimed to determine the long-term effects of oxidative stress in the testis, epididymis and spermatozoa using the rat model. Adult male rats were treated with tert-butyl hydroperoxide (t-BHP) or saline (control group), and reproductive organs and spermatozoa were collected at 3, 6, and 9 weeks after the end of treatment. We determined sperm DNA oxidation and motility, and levels of lipid peroxidation and protein expression of antioxidant enzymes in epididymis and testis. We observed that cauda epididymal spermatozoa displayed low motility and high DNA oxidation levels at all times. Lipid peroxidation was higher in caput and cauda epididymis of treated rats at 3 and 6 weeks but was similar to control levels at 9 weeks. PRDX6 was upregulated in the epididymis due to t-BHP; PRDX1 and catalase, although not significant, followed similar trend of increase. Testis of treated rats did not show signs of oxidative stress nor upregulation of antioxidant enzymes. We concluded that t-BHP-dependent oxidative stress promoted long-term changes in the epididymis and maturing spermatozoa that result in the impairment of sperm quality.

Chronic Testosterone Deprivation Sensitizes the Middle-Aged Rat Brain to Damaging Effects of Testosterone Replacement

2019 ◽  
Vol 110 (11-12) ◽  
pp. 914-928 ◽  
Author(s):  
Charity Smith ◽  
Jo Contreras-Garza ◽  
Rebecca L. Cunningham ◽  
Jessica M. Wong ◽  
Philip H. Vann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Male Rats ◽  
Testosterone Replacement ◽  
Middle Aged ◽  
Short Term ◽  
Stress Levels ◽  
Middle Aged Male

Introduction: An increasing number of middle-aged men are being screened for low testosterone levels and the number of prescriptions for various forms of testosterone replacement therapy (TRT) has increased dramatically over the last 10 years. However, the safety of TRT has come into question with some studies suggesting increased morbidity and mortality. Objective: Because the benefits of estrogen replacement in postmenopausal women and ovariectomized rodents are lost if there is an extended delay between estrogen loss and replacement, we hypothesized that TRT may also be sensitive to delayed replacement. Methods: We compared the effects of testosterone replacement after short-term (2 weeks) and long-term testosterone deprivation (LTTD; 10 weeks) in middle-aged male rats on cerebral ischemia, oxidative stress, and cognitive function. We hypothesized that LTTD would increase oxidative stress levels and abrogate the beneficial effects of TRT. Results: Hypogonadism itself and TRT after short-term castration did not affect stroke outcome compared to intact rats. However, after long-term hypogonadism in middle-aged male Fischer 344 rats, TRT exacerbated the detrimental behavioral effects of experimental focal cerebral ischemia, whereas this detrimental effect was prevented by administration of the free-radical scavenger tempol, suggesting that TRT exacerbates oxidative stress. In contrast, TRT improved cognitive performance in non-stroked rats regardless of the length of hypogonadism. In the Morris water maze, peripheral oxidative stress was highly associated with decreased cognitive ability. Conclusions: Taken together, these data suggest that TRT after long-term hypogonadism can exacerbate functional recovery after focal cerebral ischemia, but in the absence of injury can enhance cognition. Both of these effects are modulated by oxidative stress levels.

scholarly journals From Oxidative Stress to Inflammation in the Posterior Ocular Diseases: Diagnosis and Treatment

Pharmaceutics ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 1376
Author(s):  
Azza Dammak ◽  
Fernando Huete-Toral ◽  
Carlos Carpena-Torres ◽  
Alba Martin ◽  
Cristina Pastrana ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Posterior Segment ◽  
Age Related Macular Degeneration ◽  
Oxygen Species ◽  
Ocular Diseases ◽  
Protective Mechanisms ◽  
Age Related ◽  
Age Factor ◽  
Inflammatory Processes

Most irreversible blindness observed with glaucoma and retina-related ocular diseases, including age-related macular degeneration and diabetic retinopathy, have their origin in the posterior segment of the eye, making their physiopathology both complex and interconnected. In addition to the age factor, these diseases share the same mechanism disorder based essentially on oxidative stress. In this context, the imbalance between the production of reactive oxygen species (ROS) mainly by mitochondria and their elimination by protective mechanisms leads to chronic inflammation. Oxidative stress and inflammation share a close pathophysiological process, appearing simultaneously and suggesting a relationship between both mechanisms. The biochemical end point of these two biological alarming systems is the release of different biomarkers that can be used in the diagnosis. Furthermore, oxidative stress, initiating in the vulnerable tissue of the posterior segment, is closely related to mitochondrial dysfunction, apoptosis, autophagy dysfunction, and inflammation, which are involved in each disease progression. In this review, we have analyzed (1) the oxidative stress and inflammatory processes in the back of the eye, (2) the importance of biomarkers, detected in systemic or ocular fluids, for the diagnosis of eye diseases based on recent studies, and (3) the treatment of posterior ocular diseases, based on long-term clinical studies.

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