scholarly journals Cigarette Smoking and Oxidative Stress in Patients with Coronary Artery Disease

2016 ◽  
Vol 4 (4) ◽  
pp. 636-640 ◽  
Author(s):  
Gordana Kamceva ◽  
Zorica Arsova-Sarafinovska ◽  
Tatjana Ruskovska ◽  
Milka Zdravkovska ◽  
Lidija Kamceva-Panova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factor ◽  
Antioxidant Enzymes ◽  
Stress Concentration ◽  
Cigarette Smoking ◽  
Oxidative Damage ◽  
Biological Markers ◽  
Smoking Status ◽  
Significant Difference ◽  
Markers Of Oxidative Stress

AIM: To determine whether cigarette smoking, as a risk factor for CAD, affects oxidative stress.MATERIAL AND METHODS: The study included patients with CAD divided according to smoking status and number of cigarettes smoked during a whole day. In all subjects were examined biological markers of oxidative stress (concentration of oxidants and activity of antioxidant enzymes).RESULTS: The study included 300 patients with CAD, with an average age of 62.97 ± 11.18 years, with a predominance of males. Of the total, 34.0% were active smokers, and 43.0% were non-smokers. The number of the most active smokers smoked cigarettes 1-20/day. In terms of concentration of oxidants (MDA and HP) it has not proved a significant difference between smokers versus non-smokers. Over the activity of antioxidant enzymes (SOD, CAT and GPX) statistically significant difference was found in the activity of GPX and among active smokers with CAD and non-smokers with CAD (p = 0.039).CONCLUSION:Smoking as a risk factor for CAD is closely associated with increased oxidative stress and the number of cigarettes smoked plays an important role in increasing the level of oxidative damage and reduced antioxidant defence.AIM: To determine whether cigarette smoking, as a risk factor for CAD, affects (anti)oxidant status.MATERIAL AND METHODS: The study included patients with CAD, divided according to their smoking status and the number of cigarettes smoked during a day. Biological markers of oxidative stress (concentration of oxidants and activity of antioxidant enzymes) were measured in all subjects.RESULTS: The study included 300 patients with CAD, (average age of 63 ± 11 years), predominantly males. Of the total, 34.0% were active smokers, 23.0% were former smokers, and 43.0% were non-smokers. Most of the active smokers smoked 1-20 cigarettes/day. In terms of concentration of oxidants (MDA and HP) there was not a significant difference between smokers versus non-smokers. As for the activity of antioxidant enzymes (SOD, CAT and GPX), a statistically significant difference was found in the activity of GPX among the active smokers with CAD and the non-smokers with CAD (p = 0.039). CONCLUSION: Smoking as a risk factor for CAD is closely associated with increased oxidative stress, and the number of cigarettes smoked plays an important role in increasing the level of oxidative damage and reducing antioxidant defence.

Abstract WP415: Cigarette Smoking as Risk Factor for Hematoma Expansion in Primary Intracerebral Hemorrhage: Analysis From a Randomized Clinical Trial

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Shahram Majidi ◽  
Lydia Foster ◽  
Christopher P Kellner ◽  
Jose I Suarez ◽  
Adnan I Qureshi ◽  
...  
Keyword(s):  
Risk Factor ◽  
Cigarette Smoking ◽  
Intracerebral Hemorrhage ◽  
Smoking Status ◽  
Hematoma Expansion ◽  
Primary Analysis ◽  
Significant Difference ◽  
Former Smokers ◽  
Gcs Score ◽  
The Impact

Background: Cigarette smoking is a well-known risk factor for ischemic and hemorrhagic stroke. We evaluated the impact of smoking status on hematoma expansion and clinical outcome in patients with primary intracerebral hemorrhage (ICH). Methods: This is a post hoc exploratory analysis of Antihypertensive Treatment at Acute Cerebral Hemorrhage(ATACH)-2 trial. Patients with ICH were randomized into intensive blood pressure lowering(SBP: <139 mmHg) versus Baseline characteristics were compared based on smoking status. Analysis of outcome measures was adjusted for covariates included in the ATACH-2 primary analysis or those associated with smoking status. Results: Of total of 914 patients in the trial with known smoking status, 439 (48%) patients were ever-smokers (264 current smokers and 175 former smokers). Current and former smokers were younger and more likely to be male. There was no difference in the baseline Glasgow Coma Scale(GCS) score and initial hematoma size based on smoking status. Ever-smokers had higher rate of thalamic hemorrhage (42% vs 34%) and intraventricular hemorrhage (29% vs 23%); this rate was highest among former smokers (49% and 35%, respectively). Ever-smokers had higher rate of hematoma expansion in 24 hour [adjusted RR (95% CI): 1.46; (1.05 -2.03)] compared to non-smokers after adjusting for confounding factors. There was no significant difference in the rate of death and disability at 90 days between the two groups [adjusted RR; (95% CI): 1.18; (0.93 -1.50)]. Conclusions: Our analysis demonstrates cigarette smoking as an independent predictor for hematoma expansion. There was no significant difference in death and disability based on smoking status.

scholarly journals Impact of Plasma Oxidative Stress Markers on Post-race Recovery in Ultramarathon Runners: A Sex and Age Perspective Overview

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 355
Author(s):  
Carlos Guerrero ◽  
Eladio Collado-Boira ◽  
Ignacio Martinez-Navarro ◽  
Barbara Hernando ◽  
Carlos Hernando ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Antioxidant Defenses ◽  
Lipid Peroxidation Product ◽  
Finish Line ◽  
Stress Markers ◽  
Markers Of Oxidative Stress ◽  
The Impact ◽  
Plasma Markers

Oxidative stress has been widely studied in association to ultra-endurance sports. Although it is clearly demonstrated the increase in reactive oxygen species and free radicals after these extreme endurance exercises, the effects on the antioxidant defenses and the oxidative damage to macromolecules, remain to be fully clarified. Therefore, the aim of this study was to elucidate the impact of an ultramarathon race on the plasma markers of oxidative stress of 32 runners and their post-race recovery, with especial focused on sex and age effect. For this purpose, the antioxidant enzymes glutathione peroxidase (GPx) and glutathione reductase (GR) activity, as well as the lipid peroxidation product malondialdehyde (MDA) and the carbonyl groups (CG) content were measured before the race, in the finish line and 24 and 48 h after the race. We have reported an increase of the oxidative damage to lipids and proteins (MDA and CG) after the race and 48 h later. Moreover, there was an increase of the GR activity after the race. No changes were observed in runners’ plasma GPx activity throughout the study. Finally, we have observed sex and age differences regarding damage to macromolecules, but no differences were found regarding the antioxidant enzymes measured. Our results suggest that several basal plasma markers of oxidative stress might be related to the extent of muscle damage after an ultraendurance race and also might affect the muscle strength evolution.

Nonunion Rates in Hind- and Midfoot Arthrodesis in Current, Ex-, and Nonsmokers

2020 ◽  
pp. 107110072097126
Author(s):  
Jack Allport ◽  
Jayasree Ramaskandhan ◽  
Malik S. Siddique
Keyword(s):  
Risk Factor ◽  
Cohort Study ◽  
Relative Risk ◽  
Retrospective Cohort Study ◽  
Retrospective Cohort ◽  
Smoking Status ◽  
Time Frame ◽  
Modifiable Risk Factor ◽  
Level Of Evidence ◽  
Significant Difference

Background: Nonunion rates in hind or midfoot arthrodesis have been reported as high as 41%. The most notable and readily modifiable risk factor that has been identified is smoking. In 2018, 14.4% of the UK population were active smokers. We examined the effect of smoking status on union rates for a large cohort of patients undergoing hind- or midfoot arthrodesis. Methods: In total, 381 consecutive primary joint arthrodeses were identified from a single surgeon’s logbook (analysis performed on a per joint basis, with a triple fusion reported as 3 separate joints). Patients were divided based on self-reported smoking status. Primary outcome was clinical union. Delayed union, infection, and the need for ultrasound bone stimulation were secondary outcomes. Results: Smoking prevalence was 14.0%, and 32.2% were ex-smokers. Groups were comparable for sex, diabetes, and body mass index. Smokers were younger and had fewer comorbidities. Nonunion rates were higher in smokers (relative risk, 5.81; 95% CI, 2.54-13.29; P < .001) with no statistically significant difference between ex-smokers and nonsmokers. Smokers had higher rates of infection ( P = .05) and bone stimulator use ( P < .001). Among smokers, there was a trend toward slower union with heavier smoking ( P = .004). Conclusion: This large retrospective cohort study confirmed previous evidence that smoking has a considerable negative effect on union in arthrodesis. The 5.81 relative risk in a modifiable risk factor is extremely high. Arthrodesis surgery should be undertaken with extreme caution in smokers. Our study shows that after cessation of smoking, the risk returns to normal, but we were unable to quantify the time frame. Level of Evidence: Level III, retrospective cohort study.

scholarly journals Influence of Active Exposure to Tobacco Smoke on Nitric Oxide Status of Pregnant Women

2018 ◽  
Vol 15 (12) ◽  
pp. 2719 ◽  
Author(s):  
Magdalena Chełchowska ◽  
Jadwiga Ambroszkiewicz ◽  
Joanna Gajewska ◽  
Joanna Mazur ◽  
Leszek Lewandowski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Pregnant Women ◽  
Smoking Status ◽  
Multivariate Regression Analysis ◽  
Smoking During Pregnancy ◽  
Women Subjects ◽  
Total Antioxidant ◽  
Markers Of Oxidative Stress ◽  
Oxide Synthase

Smoking tobacco can impair proper vascular endothelial functioning. This is exhibited through reduced nitric oxide synthesis as well as activity due to accompanying oxidative stress. We examined the relationship between nitric oxide and markers of oxidative stress/antioxidant defense in serum of smoking and non-smoking pregnant women. Subjects included 99 healthy pregnant women, who were tested for nitric oxide (NO), endothelial (eNOS) and inducible (iNOS) nitric oxide synthase, total oxidant capacity (TOC), and total antioxidant capacity (TAC). NO, eNOS, and TAC serum concentrations were significantly lower (p < 0.005), but iNOS (p < 0.05) and TOC (p < 0.001) were higher in smokers than in non-smokers. Multivariate regression analysis showed associations between NO concentration and eNOS, TAC, and smoking status in the whole group of patients. In the model estimated separately for smokers, the highest impact of eNOS (β = 0.375; p = 0.021) and cotinine (β = −0.323; p = 0.037) was indicated for NO concentration. In the model of non-smokers, eNOS (β = 0.291, p = 0.030) and TAC (β = 0.350; p = 0.015) were important for NO level. Smoking during pregnancy could exacerbate oxidative stress, impair the action of nitric oxide synthases, and adversely affect the balance of oxygen and nitrogen metabolism. Relationships between NO concentrations and TAC in the studied women’s blood can confirm the antioxidant nature of nitric oxide.

The ethanol leaf extract of Andrographis paniculata blunts acute renal failure in cisplatin-induced injury in rats through inhibition of Kim-1 and upregulation of Nrf2 pathway

2018 ◽  
Vol 30 (2) ◽  
pp. 205-217 ◽  
Author(s):  
Bisi O. Adeoye ◽  
Ademola A. Oyagbemi ◽  
Ebunoluwa R. Asenuga ◽  
Temidayo O. Omobowale ◽  
Adeolu A. Adedapo
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Serum Creatinine ◽  
Leaf Extract ◽  
Histopathological Examination ◽  
Hematological Parameters ◽  
Kidney Tissue ◽  
Inflammatory Cells ◽  
Andrographis Paniculata ◽  
Markers Of Oxidative Stress

Abstract Background Cisplatin (CP) is a novel drug of choice in the treatment of cancer but its major limitation is nephrotoxicity, which is dose limiting. Andrographis paniculata (AP) is a common Indian dietary component. It is well known for its medicinal properties. This present study investigated the nephroprotective effect of ethanol leaf extract of Andrographis paniculata (EEAP) on CP-induced nephrotoxicity. Methods CP was used to induce nephrotoxicity in male Wistar rats to study the effect of EEAP on renal damages using hematological parameters, biochemical parameters, histology, and immunohistochemistry studies. Results The effects of EEAP were determined by CP-induced changes in different kidney tissue on antioxidant enzymes, markers of oxidative stress, serum creatinine, and urine parameters. Administration of EEAP (200 mL/kg and 400 mg/kg orally), prior to and following a single dose CP treatment (10 mg/kg i.p), significantly mitigated the CP-induced decrease in antioxidant enzymes, and increase in markers of oxidative stress, serum creatinine, and urinary protein. On histopathological examination of the kidney tissue, there was severe glomerular degeneration and infiltration of inflammatory cells in CP only treated rats, mild glomerular degeneration, and infiltration of inflammatory cells in EEAP pre-treated rats. Furthermore, EEAP activated Nrf2 and mitigated Kim-1 pathways in CP-induced nephrotoxicity. Conclusions The results showed the protective effect of EEAP against CP-induced nephrotoxicity.

scholarly journals Can plasma antioxidants prevent DNA damage in oxidative stress condition induced by growth hormone deficiency? A pilot study

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0248971
Author(s):  
Antonio Mancini ◽  
Francesco Guidi ◽  
Carmine Bruno ◽  
Flavia Angelini ◽  
Edoardo Vergani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Growth Hormone ◽  
Pilot Study ◽  
Oxidative Damage ◽  
Growth Hormone Deficiency ◽  
Hormone Deficiency ◽  
Serum Samples ◽  
Adult Growth ◽  
Significant Difference ◽  
Thymidine Glycol

Adult growth hormone deficiency (GHD), a condition characterized by increased oxidative stress, is related to augmented cardiovascular, metabolic and oncological risk. A case-control observational study has been performed to evaluate DNA oxidative damage analysing the production of thymidine-glycol in lymphocytes and its correlation with plasma antioxidant levels, evaluated as Total Antioxidant Capacity (TAC). GHD was diagnosed using GHRH 50μg iv+arginine 0,5 g/Kg test, with peak GH response <9 μg/L when BMI was <30 kg/m2 or <4 μg/L when BMI was >30 kg/m2. Three groups were identified: total GHD (n = 16), partial GHD (n = 11), and controls (n = 12). Thymidine-glycol, TAC and IGF-1 have been determined respectively in lymphocytes, plasma and serum samples. When considering thymidine-glycol, we found a significant difference between total vs partial GHD and controls. Unexpectedly thymidine-glycol was lower in total GHD, also accompanied with a significant increase in plasmatic TAC. Our results showed that in adult GHD condition, the production of antioxidant species, in response to increased oxidative stress, could exert a protective effect on thymidine-glycol formation, and consequently on DNA intracellular damages. This pilot study could be inserted in the complex scenario of oxidative damage of GHD, a subtle, yet poorly defined condition, worthy of further insights.

scholarly journals Exercise protects against doxorubicin-induced oxidative stress and proteolysis in skeletal muscle

2011 ◽  
Vol 110 (4) ◽  
pp. 935-942 ◽  
Author(s):  
Ashley J. Smuder ◽  
Andreas N. Kavazis ◽  
Kisuk Min ◽  
Scott K. Powers
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Antioxidant Enzymes ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Oxidative Damage ◽  
Muscle Fibers ◽  
Muscular Exercise ◽  
Protease Activation ◽  
Exercise Induced

Doxorubicin (Dox) is a potent antitumor agent used in cancer treatment. Unfortunately, Dox is myotoxic and results in significant reductions in skeletal muscle mass and function. Complete knowledge of the mechanism(s) by which Dox induces toxicity in skeletal muscle is incomplete, but it is established that Dox-induced toxicity is associated with increased generation of reactive oxygen species and oxidative damage within muscle fibers. Since muscular exercise promotes the expression of numerous cytoprotective proteins (e.g., antioxidant enzymes, heat shock protein 72), we hypothesized that muscular exercise will attenuate Dox-induced damage in exercise-trained muscle fibers. To test this postulate, Sprague-Dawley rats were randomly assigned to the following groups: sedentary, exercise, sedentary with Dox, or exercise with Dox. Our results show increased oxidative stress and activation of cellular proteases (calpain and caspase-3) in skeletal muscle of animals treated with Dox. Importantly, our findings reveal that exercise can prevent the Dox-induced oxidative damage and protease activation in the trained muscle. This exercise-induced protection against Dox-induced toxicity may be due, at least in part, to an exercise-induced increase in muscle levels of antioxidant enzymes and heat shock protein 72. Together, these novel results demonstrate that muscular exercise is a useful countermeasure that can protect skeletal muscle against Dox treatment-induced oxidative stress and protease activation in skeletal muscles.

scholarly journals Effect of the French Oak Wood Extract Robuvit on Markers of Oxidative Stress and Activity of Antioxidant Enzymes in Healthy Volunteers: A Pilot Study

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Martina Horvathova ◽  
Zuzana Orszaghova ◽  
Lucia Laubertova ◽  
Magdalena Vavakova ◽  
Peter Sabaka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Antioxidant Capacity ◽  
Healthy Volunteers ◽  
Total Antioxidant Capacity ◽  
Trolox Equivalent Antioxidant Capacity ◽  
Total Antioxidant ◽  
Trolox Equivalent ◽  
Markers Of Oxidative Stress

We examinedin vitroantioxidant capacity of polyphenolic extract obtained from the wood of oakQuercus robur(QR), Robuvit, using TEAC (Trolox equivalent antioxidant capacity) method and the effect of its intake on markers of oxidative stress, activity of antioxidant enzymes, and total antioxidant capacity in plasma of 20 healthy volunteers. Markers of oxidative damage to proteins, DNA, and lipids and activities of Cu/Zn-superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were determined in the erythrocytes. We have found anin vitroantioxidant capacity of Robuvit of 6.37 micromole Trolox equivalent/mg of Robuvit. One month intake of Robuvit in daily dose of 300 mg has significantly decreased the serum level of advanced oxidation protein products (AOPP) and lipid peroxides (LP). Significantly increased activities of SOD and CAT as well as total antioxidant capacity of plasma after one month intake of Robuvit have been shown. In conclusion, we have demonstrated for the first time that the intake of Robuvit is associated with decrease of markers of oxidative stress and increase of activity of antioxidant enzymes and total antioxidant capacity of plasmain vivo.

Oxidative Stress, Mitochondrial DNA Mutation, and Impairment of Antioxidant Enzymes in Aging

2002 ◽  
Vol 227 (9) ◽  
pp. 671-682 ◽  
Author(s):  
Yau-Huei Wei ◽  
Hsin-Chen Lee
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dna ◽  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Large Scale ◽  
Wide Spectrum ◽  
Radical Scavenging ◽  
Mtdna Mutations ◽  
Enhanced Production ◽  
Age Related

Mitochondria do not only produce less ATP, but they also increase the production of reactive oxygen species (ROS) as byproducts of aerobic metabolism in the aging tissues of the human and animals. It is now generally accepted that aging-associated respiratory function decline can result in enhanced production of ROS in mitochondria. Moreover, the activities of free radical-scavenging enzymes are altered in the aging process. The concurrent age-related changes of these two systems result in the elevation of oxidative stress in aging tissues. Within a certain concentration range, ROS may induce stress response of the cells by altering expression of respiratory genes to uphold the energy metabolism to rescue the cell. However, beyond the threshold, ROS may cause a wide spectrum of oxidative damage to various cellular components to result in cell death or elicit apoptosis by induction of mitochondrial membrane permeability transition and release of apoptogenic factors such as cytochrome c. Moreover, oxidative damage and large-scale deletion and duplication of mitochondrial DNA (mtDNA) have been found to increase with age in various tissues of the human. Mitochondria act like a biosensor of oxidative stress and they enable cell to undergo changes in aging and age-related diseases. On the other hand, it has recently been demonstrated that impairment in mitochondrial respiration and oxidative phosphorylation elicits an increase in oxidative stress and causes a host of mtDNA rearrangements and deletions. Here, we review work done in the past few years to support our view that oxidative stress and oxidative damage are a result of concurrent accumulation of mtDNA mutations and defective antioxidant enzymes in human aging.

Sign in / Sign up

Export Citation Format

Share Document