A manganese oxide nanozyme prevents the oxidative damage of biomolecules without affecting the endogenous antioxidant system

Nanoscale ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 3855-3863 ◽  
Author(s):  
Namrata Singh ◽  
Mohammed Azharuddin Savanur ◽  
Shubhi Srivastava ◽  
Patrick D'Silva ◽  
Govindasamy Mugesh
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Manganese Oxide ◽  
Antioxidant System ◽  
Mammalian Cells ◽  
Redox State ◽  
Stress Conditions ◽  
System P ◽  
Endogenous Antioxidant ◽  
Antioxidant Machinery

Multi-enzyme mimetic Mn3O4 nanoflowers (Mp) modulate the redox state of mammalian cells without altering the cellular antioxidant machinery under oxidative stress conditions.

scholarly journals Effects of Desiccation on Metamorphic Climax in Bombina variegata: Changes in Levels and Patterns of Oxidative Stress Parameters

Animals ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 953
Author(s):  
Tamara G. Petrović ◽  
Ana Kijanović ◽  
Nataša Kolarov Kolarov Tomašević ◽  
Jelena P. Gavrić ◽  
Svetlana G. Despotović ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Antioxidant System ◽  
Water Availability ◽  
System Control ◽  
Glutathione S Transferase ◽  
Oxidative Stress Parameters ◽  
Metamorphic Climax ◽  
Bombina Variegata ◽  
Stress Parameters

In this paper, we examined how the oxidative status (antioxidant system and oxidative damage) of Bombina variegata larvae changed during the metamorphic climax (Gosner stages: 42—beginning, 44—middle and 46—end) and compared the patterns and levels of oxidative stress parameters between individuals developing under constant water availability (control) and those developing under decreasing water availability (desiccation group). Our results revealed that larvae developing under decreasing water availability exhibited increased oxidative damage in the middle and end stages. This was followed by lower levels of glutathione in stages 44 and 46, as well as lower values of catalase, glutathione peroxidase, glutathione S-transferase and sulfhydryl groups in stage 46 (all in relation to control animals). Comparison between stages 42, 44 and 46 within treatments showed that individuals in the last stage demonstrated the highest intensities of lipid oxidative damage in both the control and desiccation groups. As for the parameters of the antioxidant system, control individuals displayed greater variety in response to changes induced by metamorphic climax than individuals exposed to desiccation treatment. The overall decrease in water availability during development led to increased oxidative stress and modifications in the pattern of AOS response to changes induced by metamorphic climax in larvae of B. variegata.

scholarly journals Melatonin reduces oxidative damage in mouse granulosa cells via restraining JNK-dependent autophagy

Reproduction ◽  
2018 ◽  
Vol 155 (3) ◽  
pp. 307-319 ◽  
Author(s):  
Yan Cao ◽  
Ming Shen ◽  
Yi Jiang ◽  
Shao-chen Sun ◽  
Honglin Liu
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Mammalian Cells ◽  
Therapeutic Strategies ◽  
Oxygen Species ◽  
Protective Effects ◽  
Follicular Atresia ◽  
Direct Role ◽  
Jnk Pathway

Oxidative stress-induced granulosa cell (GCs) injury is believed to be a common trigger for follicular atresia. Emerging evidence indicates that excessive autophagy occurs in mammalian cells with oxidative damage. N-acetyl-5-methoxytrypamine (melatonin) has been shown to prevent GCs from oxidative injury, although the exact mechanism remains to be elucidated. Here, we first demonstrated that the suppression of autophagy through the JNK/BCL-2/BECN1 signaling is engaged in melatonin-mediated GCs protection against oxidative damage. Melatonin inhibited the loss of GCs viability, formation of GFP-MAP1LC3B puncta, accumulation of MAP1LC3B-II blots, degradation of SQSTM1 and the expression of BECN1, which was correlated with impaired activation of JNK during oxidative stress. On the other hand, blocking of autophagy and/or JNK also reduced the level of H2O2-induced GCs death, but failed to further restore GCs viability in the presence of melatonin. Particularly, the suppression of autophagy provided no additional protective effects when GCs were pretreated with JNK inhibitor and/or melatonin. Importantly, we found that the enhanced interaction between BCL-2 and BECN1 might be a responsive mechanism for autophagy suppression via the melatonin/JNK pathway. Moreover, blocking the downstream antioxidant system of melatonin using specific inhibitors further confirmed a direct role of melatonin/JNK/autophagy axis in preserving GCs survival without scavenging reactive oxygen species (ROS). Taken together, our findings uncover a novel function of melatonin in preventing GCs from oxidative damage by targeting JNK-mediated autophagy, which might contribute to develop therapeutic strategies for patients with ovulation failure-related disorders.

scholarly journals Carious Lesion Severity Induces Higher Antioxidant System Activity and Consequently Reduces Oxidative Damage in Children’s Saliva

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Heitor Ceolin Araujo ◽  
Ana Cláudia Melo Stevanato Nakamune ◽  
Wilson Galhego Garcia ◽  
Juliano Pelim Pessan ◽  
Cristina Antoniali
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Oxidative Damage ◽  
Antioxidant System ◽  
Oxidative Stress Biomarkers ◽  
System Activity ◽  
Enzymatic Antioxidant ◽  
Stress Biomarkers ◽  
Salivary Biomarkers ◽  
Carious Lesions

Oxidative stress biomarkers can be found at detectable concentrations in saliva. These salivary biomarkers reflect specific oxidation pathways associated with caries and periodontitis. Our study evaluated the influence of dental caries severity (assessed using the ICCMS™ criteria) on the levels of oxidative stress biomarkers in saliva from children. Unstimulated saliva samples were collected from patients (from one to three years old) in a day care center in Birigui, SP, Brazil, two hours after fasting. Children were divided into four groups (n=30/group), according to caries severity: caries free (group A), early carious lesions (group B), moderate carious lesions (group C), and advanced carious lesions (group D). The following salivary biomarkers were determined: total proteins (TP), measured by the Lowry method; oxidative damage, measured by the TBARS method; total antioxidant capacity (TAC); superoxide dismutase (SOD) enzymatic antioxidant activity; and uric acid (UA) non-enzymatic antioxidant activity. Data were analyzed by ANOVA, followed by the Student-Newman-Keuls test, Pearson and Spearman correlation coefficients, and multivariable linear regression (p<0.05). TP, TAC, SOD enzymatic antioxidant activity, and UA non-enzymatic antioxidant activity increased with caries severity, consequently reducing salivary oxidative damage. It was concluded that higher caries severity increases salivary antioxidant system activity, with consequent reduction in salivary oxidative damage.

scholarly journals Modulations in Oxidative Stress of Erythrocytes during Bacterial and Viral Infections

2021 ◽  
Author(s):  
Vani Rajashekaraiah ◽  
Carl Hsieh ◽  
Masannagari Pallavi
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Antioxidant Capacity ◽  
Antioxidant System ◽  
Viral Infections ◽  
Physiological Properties ◽  
Biomechanical Changes ◽  
Endogenous Antioxidant ◽  
Oxidative Insult

Oxidative stress (OS) occurs when the generation of free radicals and reactive oxygen species (ROS) overwhelms the antioxidant capacity. OS causes storage lesions which can be defined as a series of biochemical and biomechanical changes. Erythrocytes are constantly exposed to OS due to the presence of ROS, which are countered by the endogenous antioxidant system. Various irreversible changes that occur include fragmentation and aggregation of proteins and lipids. The changes in proteins, lipids and antioxidant capacity are used as OS biomarkers to assess the efficacy of the erythrocytes, post oxidative insult. Aging of erythrocytes is also associated with the changes in its physical, biochemical and physiological properties and OS causes its rapid aging. Bacterial and viral infections also cause OS which alters the erythrocytes’ antioxidant capacity. These modulations in its microenvironment are both beneficial in terms of protection against invading microorganisms as well as harmful to the erythrocytes, causing damage to surrounding cells and tissues. Thus, OS biomarkers can be used to gain insights into the effects of bacterial and viral infections on the erythrocyte microenvironment.

scholarly journals Enhanced accumulation of reduced glutathione by Scopoletin improves survivability of dopaminergic neurons in Parkinson’s model

2020 ◽  
Vol 11 (9) ◽  
Author(s):  
Priyadarshika Pradhan ◽  
Olivia Majhi ◽  
Abhijit Biswas ◽  
Vinod Kumar Joshi ◽  
Devanjan Sinha
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Dopaminergic Neurons ◽  
Genetic Factors ◽  
Genetic Model ◽  
Reduced Glutathione ◽  
Redox Balance ◽  
Oxidative Markers ◽  
Cellular Inclusions ◽  
Antioxidant Machinery

Abstract Parkinson’s disease (PD) is a neuromotor disorder, primarily manifested by motor anomalies due to progressive loss of dopaminergic neurons. Although alterations in genetic factors have been linked with its etiology, exponential accumulation of environmental entities such as reactive oxygen species (ROS) initiate a cyclic chain reaction resulting in accumulation of cellular inclusions, dysfunctional mitochondria, and overwhelming of antioxidant machinery, thus accelerating disease pathogenesis. Involvement of oxidative stress in PD is further substantiated through ROS induced Parkinsonian models and elevated oxidative markers in clinical PD samples; thereby, making modulation of neuronal oxidative load as one of the major approaches in management of PD. Here we have found a potent antioxidant moiety Scopoletin (Sp), a common derivative in most of the nootropic herbs, with robust neuroprotective ability. Sp increased cellular resistance to ROS through efficient recycling of GSH to prevent oxidative damage. The Sp treated cells showed higher loads of reduced glutathione making them resistant to perturbation of antioxidant machinery or neurotoxin MPP+. Sp could restore the redox balance, mitochondrial function, and prevented oxidative damage, leading to recovery of dopaminergic neural networks and motion abilities in Drosophila genetic model of PD. Our data also suggest that Sp, in combination increases the therapeutic potency of L-DOPA by mitigating its chronic toxicity. Together, we highlight the possible ability of Sp in preventing oxidative stress mediated loss of dopaminergic neurons and at the same time enhance the efficacy of dopamine recharging regimens.

scholarly journals Protective Role of Carbonic Anhydrases III and VII in Cellular Defense Mechanisms upon Redox Unbalance

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Anna Di Fiore ◽  
Daria M. Monti ◽  
Andrea Scaloni ◽  
Giuseppina De Simone ◽  
Simona M. Monti
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Antioxidant Properties ◽  
Stress Conditions ◽  
Sulfhydryl Groups ◽  
High Rate ◽  
Molecular Surface ◽  
Carbonic Anhydrases ◽  
Cellular Defense ◽  
Functional Features

Under oxidative stress conditions, several constitutive cellular defense systems are activated, which involve both enzymatic systems and molecules with antioxidant properties such as glutathione and vitamins. In addition, proteins containing reactive sulfhydryl groups may eventually undergo reversible redox modifications whose products act as protective shields able to avoid further permanent molecular oxidative damage either in stressful conditions or under pathological circumstances. After the recovery of normal redox conditions, the reduced state of protein sulfhydryl groups is restored. In this context, carbonic anhydrases (CAs) III and VII, which are human metalloenzymes catalyzing the reversible hydration of carbon dioxide to bicarbonate and proton, have been identified to play an antioxidant role in cells where oxidative damage occurs. Both proteins are mainly localized in tissues characterized by a high rate of oxygen consumption, and contain on their molecular surface two reactive cysteine residues eventually undergoing S-glutathionylation. Here, we will provide an overview on the molecular and functional features of these proteins highlighting their implications into molecular processes occurring during oxidative stress conditions.

Thiol-based mechanisms of the thioredoxin and glutaredoxin systems: implications for diseases in the cardiovascular system

2007 ◽  
Vol 292 (3) ◽  
pp. H1227-H1236 ◽  
Author(s):  
Carsten Berndt ◽  
Christopher Horst Lillig ◽  
Arne Holmgren
Keyword(s):  
Oxidative Stress ◽  
Mammalian Cells ◽  
Redox State ◽  
Ischemia Reperfusion ◽  
Thioredoxin Reductase ◽  
Antioxidant Systems ◽  
Cardiovascular Disorders ◽  
Active Site Cysteine ◽  
Fold Family ◽  
Protein Thiols

Reactive oxygen species (ROS) and the cellular thiol redox state are crucial mediators of multiple cell processes like growth, differentiation, and apoptosis. Excessive ROS production or oxidative stress is associated with several diseases, including cardiovascular disorders like ischemia-reperfusion. To prevent ROS-induced disorders, the heart is equipped with effective antioxidant systems. Key players in defense against oxidative stress are members of the thioredoxin-fold family of proteins. Of these, thioredoxins and glutaredoxins maintain a reduced intracellular redox state in mammalian cells by the reduction of protein thiols. The reversible oxidation of Cys-Gly-Pro-Cys or Cys-Pro(Ser)-Tyr-Cys active site cysteine residues is used in reversible electron transport. Thioredoxins and glutaredoxins belong to corresponding systems consisting of NADPH, thioredoxin reductase, and thioredoxin or NADPH, glutathione reductase, glutathione, and glutaredoxin, respectively. Thioredoxin as well as glutaredoxin activities appear to be very important for the progression and severity of several cardiovascular disorders. These proteins function not only as antioxidants, they inhibit or activate apoptotic signaling molecules like apoptosis signal-regulating kinase 1 and Ras or transcription factors like NF-κB. Thioredoxin activity is regulated by the endogenous inhibitor thioredoxin-binding protein 2 (TBP-2), indicating an important role of the balance between thioredoxin and TBP-2 levels in cardiovascular diseases. In this review, we will summarize cardioprotective effects of endogenous thioredoxin and glutaredoxin systems as well as the high potential in clinical applications of exogenously applied thioredoxin or glutaredoxin or the induction of endogenous thioredoxin and glutaredoxin systems.

Sign in / Sign up

Export Citation Format

Share Document