Treadmill running prevents age-related memory deficit and alters neurotrophic factors and oxidative damage in the hippocampus of Wistar rats

2017 ◽  
Vol 334 ◽  
pp. 78-85 ◽  
Author(s):  
Cláudia Vanzella ◽  
Juliana Dalibor Neves ◽  
Adriana Fernanda Vizuete ◽  
Dirceu Aristimunha ◽  
Janaína Kolling ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Neurotrophic Factors ◽  
Wistar Rats ◽  
Memory Deficit ◽  
Treadmill Running ◽  
Age Related

scholarly journals Age-Associated Changes in Ca2+-ATPase and Oxidative Damage in Sarcoplasmic Reticulum of Rat Heart

2012 ◽  
pp. 453-460 ◽  
Author(s):  
E. BABUŠÍKOVÁ ◽  
J. LEHOTSKÝ ◽  
D. DOBROTA ◽  
P. RAČAY ◽  
P. KAPLÁN
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Oxidative Damage ◽  
Rat Heart ◽  
Wistar Rats ◽  
Sr Proteins ◽  
Oxygen Species ◽  
Protein Levels ◽  
Cardiac Contractile ◽  
Age Related ◽  
Serca 2A

Altered Ca2+ handling may be responsible for the development of cardiac contractile dysfunctions with advanced age. In the present study, we investigated the roles of oxidative damage to sarcoplasmic reticulum (SR) and expression of Ca2+-ATPase (SERCA 2a) and phospholamban in age-associated dysfunction of cardiac SR. SR vesicles were prepared from hearts of 2-, 6-, 15-, and 26-month-old Wistar rats. Although activity of Ca2+-ATPase decreased with advancing age, no differences in relative amounts of SERCA 2a and phospholamban protein were observed. On the other hand, significant accumulation of protein oxidative damage occurred with aging. The results of this study suggest that age-related alteration in Ca2+-ATPase activity in the rat heart is not a consequence of decreased protein levels of SERCA 2a and phospholamban, but could arise from oxidative modifications of SR proteins. Cellular oxidative damage caused by reactive oxygen species could contribute to age-related alternations in myocardial relaxation.

Age-related memory deficit: Role of study time and encoding strategies

2010 ◽  
Author(s):  
Charlotte Froger ◽  
Badiaa Bouazzaoui ◽  
Laurence Taconnat
Keyword(s):  
Memory Deficit ◽  
Study Time ◽  
Age Related ◽  
Encoding Strategies

Renal Cortical Slices: An In Vitro Model for Kidney Metabolism and Toxicity

1992 ◽  
Vol 20 (1) ◽  
pp. 71-76
Author(s):  
Andrea Trevisan ◽  
Stefano Maso ◽  
Paola Meneghetti
Keyword(s):  
Wistar Rats ◽  
Reduced Glutathione ◽  
Organic Anion ◽  
Cortical Slice ◽  
Lactate Dehydrogenase Release ◽  
Age Related ◽  
Renal Cortical Slice ◽  
Male Wistar Rats ◽  
Vitro Model

The in vitro renal cortical slice model was used to study: 1) the effects on the kidney of some haloalkanes and haloalkenes using 3-month-old male Wistar rats; 2) influence of age and sex on renal cortical slice indices in non-treated rats; and 3) effects of 1,2-dichloropropane on the slices after pretreatment of 3-month-old male Wistar rats with DL-butathionine-[S,R]-sulphoximine. The most nephrotoxic chemical used was 1,3-dichloropropene, which caused a total depletion in the levels of reduced glutathione, a high peroxidation of lipid (about three thousand-fold with respect to control), a significant release of tubular enzymes into the medium, and loss of organic anion ( p-aminohippurate) accumulation. All the chemicals affected the cytosol more than the brush border. The most remarkable age-related differences in the untreated slices were the progressive decrease of reduced glutathione (p<0.05 from three months of age), and an increase in lactate dehydrogenase release into the medium (p<0.05 from six months of age). By contrast, sex differences were slight. The ‘treatment with 1,2-dichloropropane of slices prepared from rats pretreated with DL-butathionine-[S,R]-sulphoximine significantly increased the depletion of glutathione content (p<0.05) and malondialdehyde release in the medium (p<0.001) caused by the solvent alone.

scholarly journals Lifelong Calorie Restriction Alleviates Age-Related Oxidative Damage in Peripheral Nerves

2010 ◽  
Vol 13 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Katherine Opalach ◽  
Sunitha Rangaraju ◽  
Irina Madorsky ◽  
Christiaan Leeuwenburgh ◽  
Lucia Notterpek
Keyword(s):  
Oxidative Damage ◽  
Calorie Restriction ◽  
Peripheral Nerves ◽  
Age Related

scholarly journals Molecular Mechanisms Responsible for Increased Vulnerability of the Ageing Oocyte to Oxidative Damage

2017 ◽  
Vol 2017 ◽  
pp. 1-22 ◽  
Author(s):  
Bettina P. Mihalas ◽  
Kate A. Redgrove ◽  
Eileen A. McLaughlin ◽  
Brett Nixon
Keyword(s):  
Oxidative Damage ◽  
Molecular Mechanisms ◽  
Spindle Assembly Checkpoint ◽  
Assisted Reproductive Technologies ◽  
Reproductive Technologies ◽  
Oocyte Quality ◽  
Protein Repair ◽  
Protective Mechanisms ◽  
Pronounced Increase ◽  
Age Related

In their midthirties, women experience a decline in fertility, coupled to a pronounced increase in the risk of aneuploidy, miscarriage, and birth defects. Although the aetiology of such pathologies are complex, a causative relationship between the age-related decline in oocyte quality and oxidative stress (OS) is now well established. What remains less certain are the molecular mechanisms governing the increased vulnerability of the aged oocyte to oxidative damage. In this review, we explore the reduced capacity of the ageing oocyte to mitigate macromolecular damage arising from oxidative insults and highlight the dramatic consequences for oocyte quality and female fertility. Indeed, while oocytes are typically endowed with a comprehensive suite of molecular mechanisms to moderate oxidative damage and thus ensure the fidelity of the germline, there is increasing recognition that the efficacy of such protective mechanisms undergoes an age-related decline. For instance, impaired reactive oxygen species metabolism, decreased DNA repair, reduced sensitivity of the spindle assembly checkpoint, and decreased capacity for protein repair and degradation collectively render the aged oocyte acutely vulnerable to OS and limits their capacity to recover from exposure to such insults. We also highlight the inadequacies of our current armoury of assisted reproductive technologies to combat age-related female infertility, emphasising the need for further research into mechanisms underpinning the functional deterioration of the ageing oocyte.

scholarly journals Sirt3 Mediates Reduction of Oxidative Damage and Prevention of Age-Related Hearing Loss under Caloric Restriction

Cell ◽  
2010 ◽  
Vol 143 (5) ◽  
pp. 802-812 ◽  
Author(s):  
Shinichi Someya ◽  
Wei Yu ◽  
William C. Hallows ◽  
Jinze Xu ◽  
James M. Vann ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Oxidative Damage ◽  
Caloric Restriction ◽  
Age Related ◽  
Age Related Hearing Loss

scholarly journals Modafinil Effects on Behavior and Oxidative Damage Parameters in Brain of Wistar Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Felipe Ornell ◽  
Samira S. Valvassori ◽  
Amanda V. Steckert ◽  
Pedro F. Deroza ◽  
Wilson R. Resende ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Open Field ◽  
Wistar Rats ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Behavioral Changes ◽  
Protein Damage ◽  
Behavioral Parameters ◽  
Carbonyl Formation ◽  
The Brain

The effects of modafinil (MD) on behavioral and oxidative damage to protein and lipid in the brain of rats were evaluated. Wistar rats were given a single administration by gavage of water or MD (75, 150, or 300 mg/kg). Behavioral parameters were evaluated in open-field apparatus 1, 2, and 3 h after drug administration. Thiobarbituric acid reactive substances (TBARS) and protein carbonyl formation were measured in the brain. MD increased locomotor activity at the highest dose 1 and 3 h after administration. MD administration at the dose of 300 mg/kg increased visits to the center of open-field 1 h after administration; however, 3 h after administration, all administered doses of MD increased visits to the open-field center. MD 300 mg/kg increased lipid damage in the amygdala, hippocampus, and striatum. Besides, MD increased protein damage in the prefrontal cortex, amygdala, and hippocampus; however, this effect varies depending on the dose administered. In contrast, the administration of MD 75 and 300 mg/kg decreased the protein damage in the striatum. This study demonstrated that the MD administration induces behavioral changes, which was depending on the dose used. In addition, the effects of MD on oxidative damage parameters seemed to be in specific brain region and doses.

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