Effect of Tai Chi Exercise on DNA Damage, Antioxidant Enzymes, and Oxidative Stress in Middle-Age Adults

2009 ◽  
Vol 6 (1) ◽  
pp. 43-54 ◽  
Author(s):  
J.A. Goon ◽  
A.H. Noor Aini ◽  
M. Musalmah ◽  
M.Y. Yasmin Anum ◽  
W.M. Wan Nazaimoon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Antioxidant Enzymes ◽  
Healthy Aging ◽  
Tai Chi ◽  
Antioxidant Defenses ◽  
Sod Activity ◽  
Tai Chi Exercise ◽  
Sedentary Subjects ◽  
Damaged Dna

Background:The biochemical mechanisms involving oxidative stress to explain the relationship between exercise and healthy aging are still unclear.Methods:Tai Chi participants and matched sedentary volunteers age 45 and above were enrolled. Glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) activities; levels of DNA damage using the comet assay; and malondialdehyde (MDA) and advanced glycation end products (AGE) were determined at 0, 6, and 12 months.Results:Tai Chi subjects had decreased normal and increased mildly damaged DNA with elevated GPx activity after 6 months (n = 25). Plasma MDA and AGE concentrations decreased significantly after 12 months (n = 15) accompanied by increased SOD activity. This may be attributed to the hormesis effect, whereby mild induction of oxidative stress at the first 6 months of exercise resulted in stimulation of antioxidant defenses. These parameters were unchanged in the sedentary subjects in the first 6 months (n = 27) except for elevated SOD activity. After 12 months, the sedentary subjects (n = 17) had decreased normal DNA and increased severely damaged DNA with unaltered MDA and AGE levels while SOD and GPx activities were significantly elevated.Conclusion:Regular Tai Chi exercise stimulated endogenous antioxidant enzymes and reduced oxidative damage markers.

scholarly journals Hepatic Postnatal Developmental Expression of Trace Mineral Associated Antioxidant Enzymes

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1077-1077
Author(s):  
Laura Sherlock ◽  
Kara Sjostrom ◽  
Nancy Krebs ◽  
Clyde Wright ◽  
Eva Nozik-Grayck
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Protein Expression ◽  
Developmental Regulation ◽  
Immune Surveillance ◽  
Developmental Expression ◽  
Antioxidant Defenses ◽  
Trace Mineral ◽  
Mrna And Protein Expression ◽  
Neonatal Liver

Abstract Objectives Oxidative stress is central to the etiology of many diseases of prematurity. Lower antioxidant defenses render premature infants vulnerable to oxidative damage secondary to infection and oxygen therapy. Antioxidant enzymes (AOE) increase perinatally in the blood and lungs. Many AOE require a micronutrient such as selenium (Se) or zinc (Zn) to function at maximum efficacy. These trace elements are low in neonates compared to adults. The liver is an important immune surveillance organ where antioxidant defense is critical for host response. It also plays a major role in micronutrient processing. However, the developmental regulation and expression of AOE in the liver is incompletely described. We hypothesized the neonatal liver would have decreased trace mineral associated AOE. Methods C57BL/6mice were sacrificed at P0, P7, P21 and 8–12 weeks. mRNA and protein expression of key AOE (SOD1, SOD2, SOD3, Gpx1, Gpx4, Msrb1, TrxR1) and factors for Se processing (Sephs2/Sps2, Scly, Pstk) were measured by qPCR and Western blot. Results Hepatic mRNA for selenoenzymes Gpx1 and Msrb1 were developmentally regulated, low at P0 and increased by adult (P < 0.05, n = 5–6). Gpx1 protein increased 7–8-fold and Msrb1 protein increased 6-fold from P0 to adult (P < 0.0001, n = 4). Gene expression of Zn related SOD1 and Mn SOD2 increased postnatally, low at P0 and increased in adult (P < 0.01 n = 5–6). Protein expression for each increased 1.5 and 3-fold from P0 to adult respectively (P < 0.001, n = 4) The mRNA and protein expression for Gpx4, TrxR1 and SOD3 remained constant postnatally. As the greatest increase was observed in selenoenzymes, factors for Se processing were evaluated. Sephs2, Scly and Pstk mRNA increased from P0 compared to P21 and adult mice (P < 0.05, n = 4–6). Protein expression for Pstk and Scly was highest at P21 and protein for Sps2 increased postnatally (P < 0.01, n = 4). Conclusions The liver experiences a postnatal increase in essential trace mineral associated AOE. Additionally, the hepatic machinery for Se processing is low in neonatal mice. We speculate that the neonatal liver is vulnerable to oxidative stress secondary to low AOE defense. We also speculate states that decreased neonatal micronutrient status may further impair the hepatic redox state. Funding Sources CCTSI Child Maternal Health Mentored Grant (L.S).

Antioxidant Responses and Lipid Peroxidation of Penaeus Indicus Postlarvae Subjected to Sublethal Copper Exposure

Crustaceana ◽  
2011 ◽  
Vol 84 (10) ◽  
pp. 1197-1210 ◽  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Copper Toxicity ◽  
Sod Activity ◽  
Lipid Peroxidation Products ◽  
Coastal Marine ◽  
Potential Biomarker ◽  
Penaeus Indicus

AbstractThe objective of this study was to determine the effect of sublethal copper concentrations on certain antioxidant enzymes and lipid peroxidation products in the postlarvae (PL) of Penaeus indicus when subjected to short- and long-term exposure in the laboratory. The PL of P. indicus were exposed to 0.1641 ppm (sublethal) copper for a period of 30 days along with a parallel control. Sampling was carried out at six different time intervals, i.e., 24, 48, and 96 hrs (shortterm), and 10, 20, and 30 days (long-term). Variations in the activity of the antioxidant enzymes, namely, catalase (CAT) and superoxide dismutase (SOD), as well as lipid peroxidation products (LPP) were measured as biomarkers of metal toxicity. Our results showed a significant (P < 0.05) increase in LPP (indicating oxidative stress) and CAT activity (indicating an adaptive response of the PL for protection against oxidative stress) in the exposed PL for all periods of exposure. However, SOD activity significantly (P < 0.05) decreased on 20 and 30 days exposure, indicating susceptibility of the PL to oxidative stress upon long-term exposure. Therefore, CAT can serve as a better biomarker of oxidative stress than SOD to long-term copper toxicity. Our results indicate that copper contamination causes oxidative stress even at sublethal doses in Penaeus indicus PL, which can thus be used as a potential biomarker of copper toxicity for long-term monitoring of coastal marine ecosystems.

scholarly journals Tai Chi Improves Oxidative Stress Response and DNA Damage/Repair in Young Sedentary Females

2014 ◽  
Vol 26 (6) ◽  
pp. 825-829 ◽  
Author(s):  
Xing-Yu Huang ◽  
Wichai Eungpinichpong ◽  
Atit Silsirivanit ◽  
Saowanee Nakmareong ◽  
Xiu-Hua Wu
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Stress Response ◽  
Tai Chi ◽  
Dna Damage Repair ◽  
Oxidative Stress Response ◽  
Damage Repair

scholarly journals Ayurvedic Amalaki Rasayana promotes improved stress tolerance and thus has anti-aging effects in Drosophila melanogaster

2016 ◽  
Author(s):  
Vibha Dwivedi ◽  
Subhash C. Lakhotia
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Drosophila Melanogaster ◽  
Stress Tolerance ◽  
Healthy Aging ◽  
Phyllanthus Emblica ◽  
Wild Type ◽  
Aging Effects ◽  
Sod Activity ◽  
Normal Food

AbstractEthnopharmacological relevanceAmalaki Rasayana (AR) is a common Ayurvedic herbal formulation of Phyllanthus emblica fruits and other ingredients and is used for general good health and healthy aging. We earlier reported it to improve life history traits and to suppress neurodegeneration as well as induced apoptosis in Drosophila.Aim of the studyTo examine effects of dietary AR supplement on cell stress responses in Drosophila melanogaster.Materials and methodsLarvae/flies, reared on normal food or on that supplemented with 0.5% (w/v) AR, were exposed to crowding, thermal or oxidative stress and examined for survival, stress tolerance and levels of lipid peroxides, SOD and HSPs.ResultsWild type larvae/flies reared on AR supplemented food survived the various cell stresses much better than those reared on normal food. AR-fed mutant park13 or DJ-1βDelta93 (Parkinson’s disease model) larvae, however, showed only partial or no protection, respectively, against paraquat-induced oxidative stress, indicating essentiality of DJ-1β for AR mediated oxidative stress tolerance. AR feeding reduced the accumulation of reactive oxygen species (ROS) and lipid peroxidation even in aged (35 day old) wild type flies while enhancing superoxide dismutase (SOD) activity. We show for the first time that while Hsp70 or Hsp83 expression under normal or stress conditions was not differentially affected by AR feeding, Hsp27 levels were elevated in AR fed wild type control as well as heat shocked larvae. Therefore, besides the known anti-oxidant activity of Phyllanthus emblica fruits, dietary AR also enhances cellular levels of Hsp27.ConclusionIn the context of the reported “anti-aging” and “healthy-aging” effects of AR, the present in vivo study on a model organisms shows that AR feeding significantly improves tolerance to a variety of cell stresses through reduced ROS and lipid peroxidation and enhanced SOD activity and Hsp27. Such improved cellular defences following dietary AR provide better homeostasis and thereby improve the life-span and quality of organism’s life.

scholarly journals The Effect of Exercise Intensity and Duration on Oxidative Stress and Antioxidant Enzymes Activity among Sedentary Healthy Adults: A Repeated Measures Study

2021 ◽  
Author(s):  
D.Maryama Ag.Daud ◽  
Fatimah Ahmedy ◽  
Dg. Marshitah Pg. Baharuddin ◽  
Tengku Fadilah Tengku Kamalden ◽  
Wan Zurinah Wan Ngah
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Exercise Intensity ◽  
Repeated Measures ◽  
Exercise Duration ◽  
Constant Load ◽  
Physiological Adaptation ◽  
Sod Activity ◽  
Oxidative Stress Status ◽  
Major Controlling Factor

Abstract Background Aerobic exercise can increase oxidative stress, but it can produce the necessary stimulus for physiological adaptation of exercise. However, the effects of intensity and duration of exercise on oxidative stress status are unclear. This study aimed to compare the effects of exercise intensity (I) and duration (D) on the oxidative stress [malondialdehyde (MDA)], and the responses of the antioxidant enzymes [catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), antioxidant enzymes ratio (AE)] among sedentary adults. Methods In a randomized crossover design, 25 sedentary adults, performed nine cycling exercise sessions with a constant load of 50%, 60% and 70% VO2peak for 10-, 20- and 30- minutes duration. Plasma MDA, CAT, GPx and SOD activity were measured before exercise (baseline) and immediately after each session (post). Results The interaction effect of intensity and duration was significant for percentage changes of MDA (FIxD=3.59, df=4, p<0.05) and CAT activity (FIxD =3.38, df=2.146, p<0.05). Repeated Measures ANOVA analysis revealed that intensity is the major controlling factor for MDA (FI =54.24, df=2, p<0.05 vs FD=8.62, df=2, p<0.05), and CAT responses (FI =14.24, df=1.619, p<0.05 vs FD = 5.96, df=1.347, p<0.05). However, the main determinant factor for SOD (FD =11.82, df=1.166, p<0.05 vs FI =5.58, df=1.289, p<0.05) and AE (FD =11.63, df=1.201, p<0.05 vs. FI =3.035, df=1.32, p>0.05) is exercise duration. Conclusions These findings suggest that exercise intensity was an essential factor of acute oxidative stress and antioxidant enzyme responses compared with the duration of exercise.

Diabetes impairs exercise training-associated thioredoxin response and glutathione status in rat brain

2009 ◽  
Vol 106 (2) ◽  
pp. 461-467 ◽  
Author(s):  
Zekine Lappalainen ◽  
Jani Lappalainen ◽  
Niku K. J. Oksala ◽  
David E. Laaksonen ◽  
Savita Khanna ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Exercise Training ◽  
Redox Status ◽  
Antioxidant Defenses ◽  
Sod Activity ◽  
Interacting Protein ◽  
Glutathione Peroxidase 1 ◽  
Thioredoxin Interacting Protein ◽  
Streptozotocin Induced Diabetes ◽  
Diabetic Brain

Regular exercise plays an important preventive and therapeutic role in oxidative stress-associated diseases such as diabetes and its complications. Thiol antioxidants including thioredoxin (TRX) and glutathione (GSH) have a crucial role in controlling cellular redox status. In this study, the effects of 8 wk of exercise training on brain TRX and GSH systems, and antioxidant enzymes were tested in rats with or without streptozotocin-induced diabetes. We found that in untrained animals, the levels of TRX-1 (TRX1) protein and activity, and thioredoxin-interacting protein (TXNip) were similar in diabetic and nondiabetic animals. Exercise training, however, increased TRX1 protein in nondiabetic animals without affecting TXNip levels, whereas diabetes inhibited the effect of training on TRX1 protein and also increased TXNip mRNA. In addition, the proportion of oxidized glutathione (GSSG) to total GSH was increased in animals with diabetes, indicating altered redox status and possibly increased oxidative stress. Glutathione peroxidase-1 (GPX1) levels were not affected by diabetes or exercise training, although diabetes increased total GPX activity. Both diabetes and exercise training decreased glutathione reductase (GRD) activity and cytosolic superoxide dismutase (Cu,Zn-SOD) levels. Nevertheless, diabetes or training had no effect on Cu,Zn-SOD mRNA, Mn-SOD protein, total SOD activity, or catalase mRNA, protein, or activity. Our findings suggest that exercise training increases TRX1 levels in brain without a concomitant rise in TXNip, and that experimental diabetes is associated with an incomplete TRX response to training. Increased oxidative stress may be both a cause and a consequence of perturbed antioxidant defenses in the diabetic brain.

Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusion

2006 ◽  
Vol 291 (6) ◽  
pp. R1756-R1763 ◽  
Author(s):  
John M. Lawler ◽  
Hyo-Bum Kwak ◽  
Wook Song ◽  
Janet L. Parker
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Antioxidant Enzymes ◽  
Exercise Training ◽  
Stress Proteins ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Sod Activity ◽  
Tnf Α

Oxidative stress is associated with muscle fatigue and weakness in skeletal muscle of ischemic heart disease patients. Recently, it was found that endurance training elevates protective heat shock proteins (HSPs) and antioxidant enzymes in skeletal muscle in healthy subjects and antioxidant enzymes in heart failure patients. However, it is unknown whether coronary ischemia and mild infarct without heart failure contributes to impairment of stress proteins and whether exercise training reverses those effects. We tested the hypothesis that exercise training would reverse alterations in muscle TNF-α, oxidative stress, HSP70, SOD (Mn-SOD, Cu,Zn-SOD), glutathione peroxidase (GPX), and catalase (CAT) due to chronic coronary occlusion of the left circumflex (CCO). Yucatan swine were divided into three groups ( n = 6 each): sedentary with CCO (SCO); 12 wk of treadmill exercise training following CCO (ECO); and sham surgery controls (sham). Forelimb muscle mass-to-body mass ratio decreased by 27% with SCO but recovered with ECO. Exercise training reduced muscle TNF-α and oxidative stress (4-hydroxynonenal adducts) caused by CCO. HSP70 levels decreased with CCO (−45%), but were higher with exercise training (+348%). Mn-SOD activity, Mn-SOD protein expression, and Cu,Zn-SOD activity levels were higher in ECO than SCO by 72, 82, and 112%, respectively. GPX activity was 177% greater in ECO than in SCO. CAT trended higher ( P = 0.059) in ECO compared with SCO. These data indicate that exercise training following onset of coronary artery occlusion results in recovery of critical stress proteins and reduces oxidative stress.

scholarly journals Aging increases Oxidative Stress and Renal Expression of Oxidant and Antioxidant Enzymes that Are Associated with an Increased Trend in Systolic Blood Pressure

2009 ◽  
Vol 2 (3) ◽  
pp. 138-145 ◽  
Author(s):  
Pedro Gomes ◽  
Sónia Simão ◽  
Elisabete Silva ◽  
Vanda Pinto ◽  
João S. Amaral ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Lipid Peroxidation ◽  
Renal Function ◽  
Antioxidant Enzymes ◽  
Systolic Blood Pressure ◽  
Renal Cortex ◽  
Antioxidant Defenses ◽  
Wky Rats ◽  
Old Rats

The aim of this study was to investigate whether the effects of aging on oxidative stress markers and expression of major oxidant and antioxidant enzymes associate with impairment of renal function and increases in blood pressure. To explore this, we determined age-associated changes in lipid peroxidation (urinary malondialdehyde), plasma and urinary hydrogen peroxide (H2O2) levels, as well as renal H2O2production, and the expression of oxidant and antioxidant enzymes in young (13 weeks) and old (52 weeks) male Wistar Kyoto (WKY) rats. Urinary lipid peroxidation levels and H2O2production by the renal cortex and medulla of old rats were higher than their young counterparts. This was accompanied by overexpression of NADPH oxidase components Nox4 and p22phoxin the renal cortex of old rats. Similarly, expression of superoxide dismutase (SOD) isoforms 2 and 3 and catalase were increased in the renal cortex from old rats. Renal function parameters (creatinine clearance and fractional excretion of sodium), diastolic blood pressure and heart rate were not affected by aging, although slight increases in systolic blood pressure were observed during this 52-week period. It is concluded that overexpression of renal Nox4 and p22phoxand the increases in renal H2O2levels in aged WKY does not associate with renal functional impairment or marked increases in blood pressure. It is hypothesized that lack of oxidative stress-associated effects in aged WKY rats may result from increases in antioxidant defenses that counteract the damaging effects of H2O2.

scholarly journals Redox Regulation in Cancer: A Double-edged Sword with Therapeutic Potential

2010 ◽  
Vol 3 (1) ◽  
pp. 23-34 ◽  
Author(s):  
Asha Acharya ◽  
Ila Das ◽  
Des Chandhok ◽  
Tapas Saha
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Significant Role ◽  
Redox Regulation ◽  
Therapeutic Potential ◽  
Redox Homeostasis ◽  
Redox System ◽  
Tumor Formation ◽  
Antioxidant Defenses ◽  
Environmental Carcinogens

Oxidative stress, implicated in the etiology of cancer, results from an imbalance in the production of reactive oxygen species (ROS) and cell’s own antioxidant defenses. ROS deregulate the redox homeostasis and promote tumor formation by initiating an aberrant induction of signaling networks that cause tumorigenesis. Ultraviolet (UV) exposures, γ-radiation and other environmental carcinogens generate ROS in the cells, which can exert apoptosis in the tumors, thereby killing the malignant cells or induce the progression of the cancer growth by blocking cellular defense system. Cancer stem cells take the advantage of the aberrant redox system and spontaneously proliferate. Oxidative stress and gene-environment interactions play a significant role in the development of breast, prostate, pancreatic and colon cancer. Prolonged lifetime exposure to estrogen is associated with several kinds of DNA damage. Oxidative stress and estrogen receptor-associated proliferative changes are suggested to play important roles in estrogen-induced breast carcinogenesis. BRCA1, a tumor suppressor against hormone responsive cancers such as breast and prostate cancer, plays a significant role in inhibiting ROS and estrogen mediated DNA damage; thereby regulate the redox homeostasis of the cells. Several transcription factors and tumor suppressors are involved during stress response such as Nrf2, NFκB and BRCA1. A promising strategy for targeting redox status of the cells is to use readily available natural substances from vegetables, fruits, herbs and spices. Many of the phytochemicals have already been identified to have chemopreventive potential, capable of intervening in carcinogenesis.

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