scholarly journals Oxidative stress action in cellular aging

2010 ◽  
Vol 53 (6) ◽  
pp. 1333-1342 ◽  
Author(s):  
Monique Cristine de Oliveira ◽  
João Paulo Ferreira Schoffen
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Aging Process ◽  
Gene Mutations ◽  
Cellular Aging ◽  
Biological Aging ◽  
Protective Measures ◽  
Beneficial Effects ◽  
Organic Systems ◽  
Chemical Residues

Various theories try to explain the biological aging by changing the functions and structure of organic systems and cells. During lifetime, free radicals in the oxidative stress lead to lipid peroxidation of cellular membranes, homeostasis imbalance, chemical residues formation, gene mutations in DNA, dysfunction of certain organelles, and the arise of diseases due to cell death and/or injury. This review describes the action of oxidative stress in the cells aging process, emphasizing the factors such as cellular oxidative damage, its consequences and the main protective measures taken to prevent or delay this process. Tests with antioxidants: vitamins A, E and C, flavonoids, carotenoids and minerals, the practice of caloric restriction and physical exercise, seeking the beneficial effects on human health, increasing longevity, reducing the level of oxidative stress, slowing the cellular senescence and origin of certain diseases, are discussed.

scholarly journals Lifelong Voluntary Exercise Modulates Age-Related Changes in Oxidative Stress

2017 ◽  
Vol 39 (01) ◽  
pp. 21-28 ◽  
Author(s):  
Mohamed Bouzid ◽  
Edith Filaire ◽  
Régis Matran ◽  
Sophie Robin ◽  
Claudine Fabre
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Lipid Peroxidation ◽  
Aging Process ◽  
Antioxidant Defense ◽  
Antioxidant Activities ◽  
Regular Physical Activity ◽  
Voluntary Exercise ◽  
Beneficial Effects ◽  
Age Related

AbstractThe hypothesis that aging and regular physical activity could influence oxidative stress has been studied by comparing antioxidant activities (superoxide dismutase (SOD), glutathione peroxidase (GPX), glutathione reductase (GR), ascorbic acid and α-Tocopherol) and malondialdehyde level (MDA) in four groups: young sedentary (n=15; age: 20.3±2.8 years; YS), young active (n=16; age: 21.4±1.9 years; YA), old sedentary (n=15; age: 65.1±3.5 years; OS) and old active (n=17; age: 67.2±4.8 years; OA). Antioxidant activities and MDA level were assessed at rest and after an incremental exercise. There was no difference in resting antioxidant activities and lipid peroxidation between YS and OS. However, resting SOD and GR activities were higher in YA compared to OA (p<0.01 and p<0.05, respectively) and resting MDA level was higher in OA compared to YA (p<0.01). After exercise, a significant increase in SOD and GPX activities was observed in YS, YA and OA (p<0.01). Likewise, after exercise a significant increase of MDA level in YA, OS and OA (p<0.01) was observed. In addition, the comparison of YA to OA and YS to OA revealed similar antioxidant activities and lipid peroxidation between YS and OA, whereas antioxidant activities were higher in YA compared to OA. These data suggest that beneficial effects of regular physical activity in antioxidant defense and lipid peroxidation damage could be impaired by the aging process and that regular physical activity in older adults could maintain age-related decreases in antioxidant defense.

scholarly journals Acrylamide Induced Oxidative Cellular Senescence in Embryonic Fibroblast Cell Line (NIH 3T3): A Protection by Carvacrol

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Mehdi Evazalipour ◽  
Pouya Safarzadeh Kozani ◽  
Pooria Safarzadeh Kozani ◽  
Sahar Shabani ◽  
Bahar Rezaei Soufi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cell Line ◽  
Cellular Senescence ◽  
Fibroblast Cell ◽  
Protective Effects ◽  
Proliferating Cells ◽  
Beneficial Effects ◽  
Nih 3T3 ◽  
Embryonic Fibroblast

Background: Stress-induced cellular senescence is a perpetual state of cell cycle arrest occurring in proliferating cells in response to stressful conditions. It is believed that oxidative stress plays a unique role in this process. As a reactive chemical compound that can induce oxidative stress, acrylamide is widely applied in several fields. Carvacrol is a liquid phenolic monoterpenoid found in essential oils of some plants and is known for its antioxidant and anticarcinogenic properties. Objectives: The current study aimed to evaluate the effects of carvacrol on oxidative stress and cellular senescence induced by acrylamide in the NIH 3T3 cell line. Methods: NIH 3T3 embryonic fibroblast cells were exposed to different concentrations of acrylamide, carvacrol, and H2O2 in a cell culture medium. The level of β-galactosidase (SA-β-gal) activity, as a marker of cellular senescence, was measured using staining and quantitative assays. Furthermore, to measure oxidative stress parameters, the content of glutathione and lipid peroxidation were determined. Results: Acrylamide could induce premature senescence evident by the elevated lipid peroxidation and SA-β-gal activity and declined cell viability and glutathione. Moreover, carvacrol showed beneficial effects on both acrylamide- and H2O2-induced cellular senescence by significantly reversing or subsiding the effect of oxidative stress and mediating its consequences. Conclusions: It can be concluded that carvacrol has protective effects against oxidative cellular senescence induced by acrylamide in the NIH 3T3 cell line.

scholarly journals Vitamin D Deficiency: Effects on Oxidative Stress, Epigenetics, Gene Regulation, and Aging

Biology ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 30 ◽  
Author(s):  
Sunil J. Wimalawansa
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Systemic Inflammation ◽  
Aging Process ◽  
Inflammatory Diseases ◽  
Cost Effective ◽  
Hypovitaminosis D ◽  
Beneficial Effects ◽  
Age Related ◽  
Mitochondrial Functions

Recent advances in vitamin D research indicate that this vitamin, a secosteroid hormone, has beneficial effects on several body systems other than the musculoskeletal system. Both 25 dihydroxy vitamin D [25(OH)2D] and its active hormonal form, 1,25-dihydroxyvitamin D [1,25(OH)2D] are essential for human physiological functions, including damping down inflammation and the excessive intracellular oxidative stresses. Vitamin D is one of the key controllers of systemic inflammation, oxidative stress and mitochondrial respiratory function, and thus, the aging process in humans. In turn, molecular and cellular actions form 1,25(OH)2D slow down oxidative stress, cell and tissue damage, and the aging process. On the other hand, hypovitaminosis D impairs mitochondrial functions, and enhances oxidative stress and systemic inflammation. The interaction of 1,25(OH)2D with its intracellular receptors modulates vitamin D–dependent gene transcription and activation of vitamin D-responsive elements, which triggers multiple second messenger systems. Thus, it is not surprising that hypovitaminosis D increases the incidence and severity of several age-related common diseases, such as metabolic disorders that are linked to oxidative stress. These include obesity, insulin resistance, type 2 diabetes, hypertension, pregnancy complications, memory disorders, osteoporosis, autoimmune diseases, certain cancers, and systemic inflammatory diseases. Vitamin D adequacy leads to less oxidative stress and improves mitochondrial and endocrine functions, reducing the risks of disorders, such as autoimmunity, infections, metabolic derangements, and impairment of DNA repair; all of this aids a healthy, graceful aging process. Vitamin D is also a potent anti-oxidant that facilitates balanced mitochondrial activities, preventing oxidative stress-related protein oxidation, lipid peroxidation, and DNA damage. New understandings of vitamin D-related advances in metabolomics, transcriptomics, epigenetics, in relation to its ability to control oxidative stress in conjunction with micronutrients, vitamins, and antioxidants, following normalization of serum 25(OH)D and tissue 1,25(OH)2D concentrations, likely to promise cost-effective better clinical outcomes in humans.

scholarly journals Oxidative stress in intensive care unit patients: a review of glutathione linked metabolism and lipid peroxidation

2019 ◽  
Vol 7 (27) ◽  
pp. 7-35
Author(s):  
Srikala Meda ◽  
Sharda Singh ◽  
Philip Palade ◽  
Sahil Tonk ◽  
Sanjay Awasthi
Keyword(s):  
Oxidative Stress ◽  
Intensive Care Unit ◽  
Lipid Peroxidation ◽  
Intensive Care ◽  
Free Radical ◽  
Critical Role ◽  
Antioxidant Defenses ◽  
Beneficial Effects ◽  
Transporter Protein ◽  
Selection Of

Despite clear evidence of increased oxidative stress in the blood and tissues of critically ill intensive care unit patients, consistent beneficial effects of many different antioxidants have not been observed, and antioxidant therapy has not yet translated into widely accepted clinical practice. The reasons for this are unclear, likely rooted in the complex and context dependent free radical behavior of antioxidants interacting with the process of lipid peroxidation. Control of lipid peroxidation is a crucial requirement for the beneficial effects of antioxidants, but the interactions of biological antioxidant defenses with the potentially harmful free radical behavior of pharmacological antioxidants complicates the dose and selection of the optimal antioxidants. Glutathione, the primary small molecule antioxidant in biological systems, is the primary enzymatic oxidative stress defense that operates in the context of glutathione-linked antioxidant enzymes to metabolize many harmful products of lipid peroxidation to mercapturic acids. Recently, the mercapturic acid transporter protein, RLIP76 (human RALBP1 gene), has been shown to have a critical role in glutathione linked oxidative stress defenses. These findings provide a rationale for new approaches towards selection and dosing of antioxidant to improve their clinical benefit.

scholarly journals Oxidative stress: Its role in regulating aging and longevity

2015 ◽  
Vol 37 (4) ◽  
pp. 16-19
Author(s):  
Catherine E. Aiken ◽  
Jane L. Tarry-Adkins ◽  
Susan E. Ozanne
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Aging Process ◽  
Cellular Level ◽  
Cellular Aging ◽  
Free Radical Damage ◽  
Early Life Environment ◽  
Cellular Components ◽  
Radical Damage

Although aging is ubiquitous across organisms, the rate at which it occurs varies considerably between species and individuals. The initial links between oxidative stress and rates of cellular aging were postulated over 50 years ago by Harman, who published a theory connecting free radical damage with the aging process in 19561. Since then a wide body of literature has accumulated demonstrating the links between oxidative damage to various cellular components and cellular senescence2. Oxidative stress is known to contribute to the aetiology of a wide variety of pathological processes including metabolic, cardiovascular and neoplastic diseases, all of which can shorten lifespan. Macromolecules such as proteins, lipids and particularly DNA can be irreversibly damaged by oxidative stress, leading to a decline in cellular function and apoptosis. This leads to aging, initially at a cellular level, then of the tissues and organs, culminating in whole organism pathology and eventually death. This article explores the various processes by which cells accrue oxidative damage and how such long-term damage leads to senescence. In particular, we focus on how the early-life environment influences the accumulation of oxidative stress over the entire life-course of an individual and how this may accelerate the normal aging process.

Changes in lipid peroxidation during pregnancy and after delivery in rats: effect of pinealectomy

Reproduction ◽  
2000 ◽  
pp. 143-149 ◽  
Author(s):  
RM Sainz ◽  
RJ Reiter ◽  
JC Mayo ◽  
J Cabrera ◽  
DX Tan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Energy Demand ◽  
Physiological State ◽  
High Energy ◽  
Free Radical Scavengers ◽  
Radical Scavengers ◽  
Oxygen Requirement ◽  
Pregnant Rats

Pregnancy is a physiological state accompanied by a high energy demand of many bodily functions and an increased oxygen requirement. Because of the increased intake and utilization of oxygen, increased levels of oxidative stress would be expected. In the present study, the degree of lipid peroxidation was examined in different tissues from non-pregnant and pregnant rats after the delivery of their young. Melatonin and other indole metabolites are known to be direct free radical scavengers and indirect antioxidants. Thus the effect of pinealectomy at 1 month before pregnancy on the accumulation of lipid damage was investigated in non-pregnant and pregnant rats after the delivery of their young. Malonaldehyde and 4-hydroxyalkenal concentrations were measured in the lung, uterus, liver, brain, kidney, thymus and spleen from intact and pinealectomized pregnant rats soon after birth of their young and at 14 and 21 days after delivery. The same parameters were also evaluated in intact and pinealectomized non-pregnant rats. Shortly after delivery, lipid oxidative damage was increased in lung, uterus, brain, kidney and thymus of the mothers. No differences were detected in liver and spleen. Pinealectomy enhanced this effect in the uterus and lung. It is concluded that during pregnancy high levels of oxidative stress induce an increase in oxidative damage to lipids, which in some cases is inhibited by the antioxidative actions of pineal indoles.

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome

2011 ◽  
Vol 14 (3) ◽  
pp. 443-448 ◽  
Author(s):  
N. Kurhalyuk ◽  
H. Tkachenko ◽  
K. Pałczyńska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Brown Trout ◽  
Salmo Trutta ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Reactive Substance ◽  
Brown Trout Salmo Trutta

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome In the present work we evaluated the effect of ulcerative dermal necrosis (UDN) syndrome on resistance of erythrocytes to haemolytic agents and lipid peroxidation level in the blood from brown trout (Salmo trutta m. trutta L.). Results showed that lipid peroxidation increased in erythrocytes, as evidenced by high thiobarbituric acid reactive substance (TBARS) levels. Compared to control group, the resistance of erythrocytes to haemolytic agents was significantly lower in UDN-positive fish. Besides, UDN increased the percent of hemolysated erythrocytes subjected to the hydrochloric acid, urea and hydrogen peroxide. Results showed that UDN led to an oxidative stress in erythrocytes able to induce enhanced lipid peroxidation level, as suggested by TBARS level and decrease of erythrocytes resistance to haemolytic agents.

Pharmacological study on the possible involvement of a Nrf2 -Heme oxygenase pathways in anti-cataract activity of fisetin

2020 ◽  
Vol 10 (1) ◽  
pp. 14-19
Author(s):  
Krishna Reddy BV ◽  
Avinash Kumar Reddy G ◽  
Sujitha V ◽  
Manasa A
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Pharmacological Study ◽  
World Population ◽  
Central Feature ◽  
Beneficial Effects ◽  
Radical Production ◽  
Anti Oxidant ◽  
Diabetic Population ◽  
Oxidant Status

DM otherwise diabetes is now a days an epidemic with the percentage of patient population rising to almost 10% of the world population. Out of all the DM complications, cataract leads the way contributing to disabilities to about 60% of diabetic population. But the pathogenesis of DM cataract is still a half-understood area of medicine there by posing a problem in the therapy. The data that we have till now gives us enough evidence to advocate the oxidative stress has a major role for the pathogenesis of DM complications like DMnephropathy, DMneuropathy, and cardiac hypertrophy, which suggests the oxidative stress is a central feature of diabetes. In the current research, the pharmacological evaluation of Fisetin for its DM based anti-cataract property was performed. This research concentrates to estimate the possible involvement of Nrf-2 / heme oxygenase (HO)-pathway in the observed therapeutic effect, if any. The data obtained in this study also indicate that the observed beneficial effects mainly due to activation of Nrf2/HO-1 pathway. These effects probably result in increased tissue anti-oxidant status as well as decreased free radical production, which ultimately responsible for the observed beneficial effects of Fisetin against hyperglycemia-induced cataract.

Safety of Antitheilerial Drug Buparvaquone in Rams

2018 ◽  
Vol 46 (1) ◽  
Author(s):  
Nermin Isik ◽  
Ozlem Derinbay Ekici ◽  
Ceylan Ilhan ◽  
Devran Coskun
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Alkaline Phosphatase ◽  
Blood Cell ◽  
Blood Urea Nitrogen ◽  
Troponin I ◽  
Oxidative Status ◽  
Blood Samples ◽  
Heart Damage

 Background: Theileriosis is a tick-borne disease caused by Theileria strains of the protozoan species. Buparvaquone is the mostly preferred drug in the treatment theileriosis, while it is safety in sheep, has not been detailed investigated. It has been hypothesized that buparvaquone may show side effects and these effects may be defined some parameters measured from blood in sheep when it is used at the recommended dose and duration. The aim of this research was to determine the effect of buparvaquone on the blood oxidative status, cardiac, hepatic and renal damage and bone marrow function markers.Materials, Methods & Results: In this study, ten adult (> 2 years) Akkaraman rams were used. Healthy rams were placed in paddocks, provided water ad libitum, and fed with appropriate rations during the experiment. Buparvaquone was ad­ministered at the dose of 2.5 mg/kg (IM) intramuscularly twice at 3-day intervals. Blood samples were obtained before (0. h, Control) and after drug administration at 0.25, 0.5, 1, 2, 3, 4 and 5 days. The blood samples were transferred to gel tubes, and the sera were removed (2000 g, 15 min). During the study, the heart rate, respiratory rate, and body temperature were measured at each sampling time. In addition, the animals were clinically observed. Plasma oxidative status mark­ers (Malondialdehyde, total antioxidant status, catalase, glutathione peroxidase, superoxide dismutase), serum cardiac (Troponin I, creatine kinase-MBmass, lactate dehydrogenase), hepatic (Alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, gamma glutamyltransferase, total protein, albumin, globulin) and renal (Creatinine, blood urea nitrogen) damage markers and hemogram values (white blood cell, red blood cell, platelet, hemogram, hematocrit) were measured. Buparvaquone caused statistically significantly (P < 0.05) increases in the troponin I and blood urea nitrogen levels and fluctuations in alkaline phosphatase activity, but there was no any statistically significance difference determined in the other parameters.Discussion: In this study, buparvaquone was administered two times at a dose of 2.5 mg/kg (IM) at 3-day intervals. Al­though the result was not statistically significant (P > 0.05), it was determined that buparvaquone gradually increased the levels of the main oxidative stress marker, MDA, by approximately 2.8 fold. CAT and GPX levels were also found to have decreased by 2.2 fold. Buparvaquone may cause lipid peroxidation by producing free radicals. Some other antiprotozoal drugs may affect the oxidative status and may increase MDA level and decrease SOD level. In this study, MDA, which is an indicator of lipid peroxidation in vivo, was used to partially detect developing lipid peroxidation. Changes in the levels of reduced GPX and CAT enzymes could be attributed to their use in mediating the hydrogen peroxide detoxification mechanisms. The absence of significant changes in the TAS levels in this study suggests that buparvaquone may partially induce oxidative stress by producing hydrogen peroxide, but no significant changes occurred in the oxidative stress level because of the high antioxidant capacity of sheep. In this study, buparvaquone caused a statistically significant increase (P < 0.05) in the level of Tn-I, which is a marker of specific cardiac damage (P < 0.05), whereas there was no statistically (P > 0.05) significant increase in CK-MBmass. Tn-I and CK-MB levels, which are used to define heart damage in humans, have been successfully used to determine heart damage in sheep. In this research study, the statistically significant increases in Tn-I but not CK-MBmass levels could be considered indicative of mild cardiac damage.Keywords: ram, buparvaquone, safety.

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