scholarly journals Impact of Oxidative Stress on Inflammation in Rheumatoid and Adjuvant Arthritis: Damage to Lipids, Proteins, and Enzymatic Antioxidant Defense in Plasma and Different Tissues

2020 ◽  
Author(s):  
Silvester Ponist ◽  
Miloslav Zloh ◽  
Katarina Bauerova
Keyword(s):  
Oxidative Stress ◽  
Adjuvant Arthritis ◽  
Antioxidant Defense ◽  
Enzymatic Antioxidant ◽  
Different Tissues

scholarly journals Antioxidant Capacity of Preterm Neonates Assessed by Hydrogen Donor Value

Medicina ◽  
2019 ◽  
Vol 55 (11) ◽  
pp. 720 ◽  
Author(s):  
Melinda Matyas ◽  
Monica G. Hasmasanu ◽  
Gabriela Zaharie
Keyword(s):  
Oxidative Stress ◽  
Respiratory Distress ◽  
Antioxidant Capacity ◽  
Antioxidant Defense ◽  
Hydrogen Donor ◽  
Study Group ◽  
Enzymatic Antioxidants ◽  
Premature Newborns ◽  
Enzymatic Antioxidant ◽  
Hydrogen Donors

Background and objectives: Premature newborns have a number of oxidative stress-inducing disorders. Antioxidant defense is deficient in premature newborns. Hydrogen donors can be used to evaluate the non-enzymatic antioxidant defense. By measuring hydrogen donors, a group of antioxidants can be assessed: tocopherol, ascorbic acid, and glutathione. These represent the most relevant group of non-enzymatic antioxidants. The main aim of this study was to evaluate the non-enzymatic antioxidant defense capacity of premature newborns by measuring hydrogen donors. Materials and Methods: We evaluated the non-enzymatic antioxidant capacity by hydrogen donor measurement in 24 premature newborns with various oxidative stress-inducing disorders and in 14 premature newborns without oxidative stress-inducing conditions. Statistical analysis was performed using the Statistica program (v. 8, StatSoft, Round Rock, TX, USA). Differences between groups were tested with Wilcoxon matched test for quantitative paired data or Mann–Whitney test for quantitative independent data. The Z test for proportions was used to compare qualitative data among subgroups. Results: Hydrogen donors in the study group had a significantly lower value on the first day of life compared to the value of the control group. Also, the hydrogen donor value in the study group was significantly lower on the first day compared to the third day of life (p < 0.05). Neonates with mild respiratory distress (14 cases) had increased hydrogen donor values on their third day of life compared to the first day of life. Conclusions: The antioxidant capacity is influenced by oxidative stress-inducing disorders. Respiratory distress influenced the hydrogen donor value and antioxidant defense. Antioxidant defense gradually improves after birth according to gestational age.

scholarly journals Endogenous Enzymatic Antioxidant Defense and Pathologies

2021 ◽  
Author(s):  
Atika Eddaikra ◽  
Naouel Eddaikra
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Redox Balance ◽  
Biological Macromolecules ◽  
Metabolic Dysfunction ◽  
Enzymatic Antioxidant ◽  
Metabolic Imbalance

Oxidative stress is an important component of various diseases. It manifests as an imbalance caused by an excessive production of reactive oxygen species (ROS) which are associated with a deficit of antioxidant activity. This deficit can be the consequence of genetic factors, environmental ones, metabolic imbalance, toxicity or direct attacks by the accumulation of free radicals. These can induce metabolic dysfunction affecting biological macromolecules in their structures or activities. From a physiological perspective, the neutralization of free radicals is ensured by enzymatic, antioxidant and non-enzymatic defense systems. In the present chapter, we will focus on the endogenous enzymatic antioxidant defense system such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPxs), thioredoxin (Trx) and paraxonase which play an important role in homeostatic redox balance. Also, we will review this set of antioxidants enzymes within different pathological states such as diabetes, cancer, autoimmune diseases, cardiovascular, Alzheimer’s, Parkinson’s or parasitic diseases such as Leishmaniasis and Malaria.

scholarly journals Are insulin-resistance and oxidative stress cause or consequence of aging

2020 ◽  
Vol 245 (14) ◽  
pp. 1260-1267
Author(s):  
Sylwia Dzięgielewska-Gęsiak ◽  
Dorota Stołtny ◽  
Alicja Brożek ◽  
Małgorzata Muc-Wierzgoń ◽  
Ewa Wysocka
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Antioxidant Status ◽  
Antioxidant Defense ◽  
Total Antioxidant Status ◽  
Thiobarbituric Acid ◽  
Elderly Individuals ◽  
Total Antioxidant ◽  
Antioxidant Defense Systems ◽  
Antioxidant Markers

Insulin resistance (IR) may be associated with oxidative stress and leads to cardiovascular disorders. Current research focuses on interplay between insulin-resistance indices and oxidant-antioxidant markers in elderly individuals with or without insulin-resistance. The assessment involved anthropometric data (weight, height, BMI, percentage of body fat (FAT)) and biochemical tests (glucose, lipids, serum insulin and plasma oxidant-antioxidant markers: Thiobarbituric Acid-Reacting Substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1) and total antioxidant status). Insulin resistance index (IR) assuming a cut-off point of 0.3 allows to divides groups into: insulin sensitive group (InsS) IR < 0,3 ( n = 35, median age 69.0 years) and insulin-resistant group (InsR) IR ≥ 0.3 ( n = 51, median age 71.0 years). Lipids and antioxidant defense system markers did not differentiate the investigated groups. In the InsR elderly group, the FAT was increased ( P < 0.000003) and TBARS ( P = 0.008) concentration decreased in comparison with InsS group. A positive correlation for SOD-1 and total antioxidant status ( P < 0.05; r =  0.434) and a negative correlation for TBARS and age ( P < 0.05 with r = −0.421) were calculated in InsR individuals. In elderly individuals, oxidative stress persists irrespective of insulin-resistance status. We suggest that increased oxidative stress may be consequence of old age. An insulin action identifies those at high risk for atherosclerosis, via congruent associations with oxidative stress and extra- and intra-cellular antioxidant defense systems. Thus, we maintain that insulin-resistance is not the cause of aging. Impact statement Insulin resistance is associated with oxidative stress leading to cardiovascular diseases. However, little research has been performed examining elderly individuals with or without insulin-resistance. We demonstrate that antioxidant defense systems alone is not able to abrogate insulin action in elderly individuals at high risk for atherosclerosis, whereas the combined oxidant-antioxidant markers (thiobarbituric acid-reacting substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1), and total antioxidant status (TAS)) might be more efficient and perhaps produce better clinical outcome. In fact, a decrease in oxidative stress and strong interaction between antioxidant defense can be seen only among insulin-resistant elderly individuals. This is, in our opinion, valuable information for clinicians, since insulin-resistance is considered strong cardiovascular risk factor.

Skeletal muscle uncoupling-induced longevity in mice is linked to increased substrate metabolism and induction of the endogenous antioxidant defense system

2013 ◽  
Vol 304 (5) ◽  
pp. E495-E506 ◽  
Author(s):  
S. Keipert ◽  
M. Ost ◽  
A. Chadt ◽  
A. Voigt ◽  
V. Ayala ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Mapk Signaling ◽  
Redox Signaling ◽  
Defense System ◽  
High Fat ◽  
Substrate Metabolism ◽  
Endogenous Antioxidant

Ectopic expression of uncoupling protein 1 (UCP1) in skeletal muscle (SM) mitochondria increases lifespan considerably in high-fat diet-fed UCP1 Tg mice compared with wild types (WT). To clarify the underlying mechanisms, we investigated substrate metabolism as well as oxidative stress damage and antioxidant defense in SM of low-fat- and high-fat-fed mice. Tg mice showed an increased protein expression of phosphorylated AMP-activated protein kinase, markers of lipid turnover (p-ACC, FAT/CD36), and an increased SM ex vivo fatty acid oxidation. Surprisingly, UCP1 Tg mice showed elevated lipid peroxidative protein modifications with no changes in glycoxidation or direct protein oxidation. This was paralleled by an induction of catalase and superoxide dismutase activity, an increased redox signaling (MAPK signaling pathway), and increased expression of stress-protective heat shock protein 25. We conclude that increased skeletal muscle mitochondrial uncoupling in vivo does not reduce the oxidative stress status in the muscle cell. Moreover, it increases lipid metabolism and reactive lipid-derived carbonyls. This stress induction in turn increases the endogenous antioxidant defense system and redox signaling. Altogether, our data argue for an adaptive role of reactive species as essential signaling molecules for health and longevity.

Impact of seasonally frozen soil on germinability and antioxidant enzyme activity of Picea asperata seeds

2009 ◽  
Vol 39 (4) ◽  
pp. 723-730 ◽  
Author(s):  
Jihong Qin ◽  
Qing Liu
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Defense ◽  
Germination Rate ◽  
Antioxidant Defense System ◽  
Antioxidant Enzyme Activity ◽  
Frozen Soil ◽  
Defense System ◽  
Frozen Ground ◽  
Subalpine Zone ◽  
Picea Asperata

In the subalpine zone of the Qinghai–Tibetan Plateau of China, Dragon spruce (Picea asperata Mast.) is commonly used for reforestation. The aim of the present work was to study the effects of seasonally frozen soil on the germination of P. asperata seeds and to investigate whether these effects were associated with resumption of the antioxidant defense system. The nonfrozen treatment resulted in near failure of germination (1%) and was associated with relatively high levels of hydrogen peroxide (H2O2) and low activities of superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxide (APX). Germination of P. asperata seeds at 10 cm under the seasonally frozen soil was higher than that at 5 cm by 26%; this higher germination rate was associated with the recovery of SOD, CAT, and APX activities. The levels of malondialdehyde (MDA) in seeds from seasonally frozen treatments were higher than those in the nonfrozen treatment, implying greater lipid peroxidation and that frozen seeds might have suffered from oxidative stress. The results indicate that seasonally frozen soil facilitated the germination of P. asperata seeds and that germination was closely related to the resumption of antioxidant enzymes activity. Overall, these findings suggest that the disappearance of seasonally frozen ground caused by global warming might result in failure of regeneration of P. asperata.

Impact of CuO nanoparticles on maize: Comparison with CuO bulk particles with special reference to oxidative stress damages and antioxidant defense status

Chemosphere ◽  
2022 ◽  
Vol 287 ◽  
pp. 131911
Author(s):  
Doyel Roy ◽  
Sinchan Adhikari ◽  
Ayan Adhikari ◽  
Supriya Ghosh ◽  
Ikbal Azahar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Special Reference ◽  
Antioxidant Defense ◽  
Cuo Nanoparticles

scholarly journals Identification of Redox-Sensitive Transcription Factors as Markers of Malignant Pleural Mesothelioma

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1138
Author(s):  
Martina Schiavello ◽  
Elena Gazzano ◽  
Loredana Bergandi ◽  
Francesca Silvagno ◽  
Roberta Libener ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Malignant Pleural Mesothelioma ◽  
Antioxidant Defense ◽  
Asbestos Exposure ◽  
Predictive Biomarkers ◽  
Antioxidant Systems ◽  
Pleural Mesothelioma ◽  
Related Factor ◽  
Aggressive Cancer

Although asbestos has been banned in most countries around the world, malignant pleural mesothelioma (MPM) is a current problem. MPM is an aggressive tumor with a poor prognosis, so it is crucial to identify new markers in the preventive field. Asbestos exposure induces oxidative stress and its carcinogenesis has been linked to a strong oxidative damage, event counteracted by antioxidant systems at the pulmonary level. The present study has been focused on some redox-sensitive transcription factors that regulate cellular antioxidant defense and are overexpressed in many tumors, such as Nrf2 (Nuclear factor erythroid 2-related factor 2), Ref-1 (Redox effector factor 1), and FOXM1 (Forkhead box protein M1). The research was performed in human mesothelial and MPM cells. Our results have clearly demonstrated an overexpression of Nrf2, Ref-1, and FOXM1 in mesothelioma towards mesothelium, and a consequent activation of downstream genes controlled by these factors, which in turn regulates antioxidant defense. This event is mediated by oxidative free radicals produced when mesothelial cells are exposed to asbestos fibers. We observed an increased expression of Nrf2, Ref-1, and FOXM1 towards untreated cells, confirming asbestos as the mediator of oxidative stress evoked at the mesothelium level. These factors can therefore be considered predictive biomarkers of MPM and potential pharmacological targets in the treatment of this aggressive cancer.

Mechanisms of Liver Injury. III. Oxidative stress in the pathogenesis of hepatitis C virus

2006 ◽  
Vol 290 (5) ◽  
pp. G847-G851 ◽  
Author(s):  
Jinah Choi ◽  
J.-H. James Ou
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Liver Injury ◽  
Iron Overload ◽  
Antioxidant Defense ◽  
Hcv Infection ◽  
Nitrogen Species ◽  
Systemic Oxidative Stress

Hepatitis C virus (HCV) is a major cause of viral hepatitis that can progress to hepatic fibrosis, steatosis, hepatocellular carcinoma, and liver failure. HCV infection is characterized by a systemic oxidative stress that is most likely caused by a combination of chronic inflammation, iron overload, liver damage, and proteins encoded by HCV. The increased generation of reactive oxygen and nitrogen species, together with the decreased antioxidant defense, promotes the development and progression of hepatic and extrahepatic complications of HCV infection. This review discusses the possible mechanisms of HCV-induced oxidative stress and its role in HCV pathogenesis.

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