Abstract
Excess reactive oxygen species (ROS) generation and oxidative stress in vascular tissue is associated with many diseases. Glutathione (GSH), one of the most abundant low molecular weight non-protein thiols, modulates physiological levels of ROS and is involved in the cell’s oxidative stress response. The GSH/GSSG redox couple is commonly used in measuring oxidative stress status. The imbalance of GSH is reported in many disease states including atherosclerosis, cancer, neurodegenerative disease, and aging. The importance of GSH in modulation of intracellular ROS involves both its protective defense against the damaging effects of oxidative stress and its role in facilitating ROS cell signaling. In this paper, we review significant results obtained from mass balance and kinetic reactions based computational and mathematical models of GSH participation in oxidative stress. The focus is on the mediation of ROS and oxidative stress with respect to the antioxidant capacity of the cell. We discuss the role of GSH in the redox state of the cell, maintaining homeostasis through GSH synthesis, scavenging of free radicals, modulating hydrogen peroxide level and interacting with nitric oxide pathways.
Keywords: Biotransport models, kinetic models, glutathione peroxidase, glutathione reductase, protein s-glutathionylation, nitrosylation, hydrogen peroxide
Current Neurovascular Research
Title:Computational Insights into the Role of Glutathione in Oxidative Stress
Volume: 10 Issue: 2
Author(s): Caitlin E. Presnell, Gaurav Bhatti, Lidya S. Numan, Mitchell Lerche, Salem K. Alkhateeb, Muhannad Ghalib, Mohammed Shammaa and Mahendra Kavdia
Affiliation:
Keywords: Biotransport models, kinetic models, glutathione peroxidase, glutathione reductase, protein s-glutathionylation, nitrosylation, hydrogen peroxide
Abstract: Excess reactive oxygen species (ROS) generation and oxidative stress in vascular tissue is associated with many diseases. Glutathione (GSH), one of the most abundant low molecular weight non-protein thiols, modulates physiological levels of ROS and is involved in the cell’s oxidative stress response. The GSH/GSSG redox couple is commonly used in measuring oxidative stress status. The imbalance of GSH is reported in many disease states including atherosclerosis, cancer, neurodegenerative disease, and aging. The importance of GSH in modulation of intracellular ROS involves both its protective defense against the damaging effects of oxidative stress and its role in facilitating ROS cell signaling. In this paper, we review significant results obtained from mass balance and kinetic reactions based computational and mathematical models of GSH participation in oxidative stress. The focus is on the mediation of ROS and oxidative stress with respect to the antioxidant capacity of the cell. We discuss the role of GSH in the redox state of the cell, maintaining homeostasis through GSH synthesis, scavenging of free radicals, modulating hydrogen peroxide level and interacting with nitric oxide pathways.
Export Options
About this article
Cite this article as:
E. Presnell Caitlin, Bhatti Gaurav, S. Numan Lidya, Lerche Mitchell, K. Alkhateeb Salem, Ghalib Muhannad, Shammaa Mohammed and Kavdia Mahendra, Computational Insights into the Role of Glutathione in Oxidative Stress, Current Neurovascular Research 2013; 10 (2) . https://dx.doi.org/10.2174/1567202611310020011
DOI https://dx.doi.org/10.2174/1567202611310020011 |
Print ISSN 1567-2026 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5739 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Molecular Analysis of the In Vivo Metabolism and Biodistribution of Metabolically and Non-Metabolically Activated Combi-Molecules of the Triazene Class
Drug Metabolism Letters Editorial :
Recent Patents on CNS Drug Discovery (Discontinued) Influence of Aldo-keto Reductase 1C3 in Prostate Cancer - A Mini Review
Current Cancer Drug Targets Anti-Cancer Phytometabolites Targeting Cancer Stem Cells
Current Genomics Recent Developments in Taxane Drug Delivery
Current Drug Delivery Functional Role of miR-34 Family in Human Cancer
Current Drug Targets Role of Tumor Microenvironment in Cancer Stem Cells Resistance to Radiotherapy
Current Cancer Drug Targets Blood-Brain Barrier Transport of Drugs for the Treatment of Brain Diseases
CNS & Neurological Disorders - Drug Targets Potential Impacts of Prebiotics and Probiotics on Cancer Prevention
Anti-Cancer Agents in Medicinal Chemistry Potential Therapeutic Targets in Energy Metabolism Pathways of Breast Cancer
Current Cancer Drug Targets Targeting Epigenetics in Nervous System Disease
CNS & Neurological Disorders - Drug Targets Molecular Targeted Approaches to Cancer Therapy and Prevention Using Chalcones
Current Cancer Drug Targets Structural Basis and Therapeutic Implication of the Interaction of CCN Proteins with Glycoconjugates
Current Pharmaceutical Design Phospholipase A2 Isoforms as Novel Targets for Prevention and Treatment of Inflammatory and Oncologic Diseases
Current Drug Targets Epigenome-Wide Association Studies (EWAS) in Cancer
Current Genomics Molecular Pathways Involved in Apoptotic Cell Death in the Injured Cochlea: Cues to Novel Therapeutic Strategies
Current Pharmaceutical Design Viral Vectors for Cancer Gene Therapy: Viral Dissemination and Tumor Targeting
Current Gene Therapy Heat Shock Proteins in Cancer: Signaling Pathways, Tumor Markers and Molecular Targets in Liver Malignancy
Protein & Peptide Letters Medicinal Compound Celastrol As a Potential Clinical Anticancer Drug: Lessons Learned From Preclinical Studies
Clinical Cancer Drugs APE1/Ref-1Role in Redox Signaling: Translational Applications of Targeting the Redox Function of the DNA Repair/Redox Protein APE1/Ref-1
Current Molecular Pharmacology