ArticleJournal of virology2006
Retrovirus-induced oxidative stress with neuroimmunodegeneration is suppressed by antioxidant treatment with a refined monosodium alpha-luminol (Galavit).
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- A Study on the Planarian Model Confirms the Antioxidant Properties of Tameron against X-ray- and Menadione-Induced Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Article
- Pathophysiological basis and promise of experimental therapies for Gulf War Illness, a chronic neuropsychiatric syndrome in veterans.Psychopharmacology · 2023Review
- PI3K/Akt/Nrf2 mediated cellular signaling and virus-host interactions: latest updates on the potential therapeutic management of SARS-CoV-2 infection.Frontiers in molecular biosciences · 2023Review
- Gulf War Illness: Mechanisms Underlying Brain Dysfunction and Promising Therapeutic Strategies.Pharmacology & therapeutics · 2021Review
- Strategies for Targeting SARS CoV-2: Small Molecule Inhibitors-The Current Status.Frontiers in immunology · 2020Review
- Monosodium luminol reinstates redox homeostasis, improves cognition, mood and neurogenesis, and alleviates neuro- and systemic inflammation in a model of Gulf War Illness.Redox biology · 2020Article
- Therapeutic Modulation of Virus-Induced Oxidative Stress via the Nrf2-Dependent Antioxidative Pathway.Oxidative medicine and cellular longevity · 2018Review
- Cytoplasmic vacuolization in cell death and survival.Oncotarget · 2016Review
- p53 as a retrovirus-induced oxidative stress modulator.The Journal of general virology · 2015Article
- ROS upregulation during the early phase of retroviral infection plays an important role in viral establishment in the host cell.The Journal of general virology · 2013Article
- Oxidative stress and potential applications of free radical scavengers in glaucoma.Redox report : communications in free radical research · 2013Review
- Activation of AMP-activated protein kinase in cerebella of Atm-/- mice is attributable to accumulation of reactive oxygen species.Biochemical and biophysical research communications · 2012Article
- MoMuLV-ts-1: A Unique Mouse Model of Retrovirus-Induced Lymphoma Transmitted by Breast Milk.Advances in virology · 2011Article
- Phenylbutyric acid suppresses protein accumulation-mediated ER stress in retrovirus-infected astrocytes and delays onset of paralysis in infected mice.Neurochemistry international · 2010Article
- Attenuation of oxidative stress, inflammation and apoptosis by minocycline prevents retrovirus-induced neurodegeneration in mice.Brain research · 2009Article
- The Nrf2-ARE cytoprotective pathway in astrocytes.Expert reviews in molecular medicine · 2009Review
- The degree of folding instability of the envelope protein of a neurovirulent murine retrovirus correlates with the severity of the neurological disease.Journal of virology · 2009Article
- Oxidative stress is linked to ERK1/2-p16 signaling-mediated growth defect in ATM-deficient astrocytes.The Journal of biological chemistry · 2009Article
- Inflammation and oxidative stress in vertebrate host-parasite systems.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2009Review
- The ubiquitin-proteasome system in spongiform degenerative disorders.Biochimica et biophysica acta · 2008Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress is involved in many human neuroimmunodegenerative diseases, including human immunodeficiency virus disease/AIDS. The retrovirus ts1, a mutant of Moloney murine leukemia virus, causes oxidative stress and progressive neuro- and immunopathology in mice infected soon after birth. These pathological changes include spongiform neurodegeneration, astrogliosis, thymic atrophy, and T-cell depletion. Astrocytes and thymocytes are directly infected and killed by ts1. Neurons are not infected, but they also die, most likely as an indirect result of local glial infection. Cytopathic effects of ts1 infection in cultured astrocytes are associated with accumulation of the viral envelope precursor protein gPr80env in the endoplasmic reticulum (ER), which triggers ER stress and oxidative stress. We have reported (i) that activation of the Nrf2 transcription factor and upregulation of antioxidative defenses occurs in astrocytes infected with ts1 in vitro and (ii) that some ts1-infected astrocytes survive infection by mobilization of these pathways. Here, we show that treatment with a refined monosodium alpha-luminol (Galavit; GVT) suppresses oxidative stress and Nrf2 activation in cultured ts1-infected astrocytes. GVT treatment also inhibits the development of spongiform encephalopathy and gliosis in the central nervous system (CNS) in ts1-infected mice, preserves normal cytoarchitecture in the thymus, and delays paralysis, thymic atrophy, wasting, and death. GVT treatment of infected mice reduces ts1-induced oxidative stress, cell death, and pathogenesis in both the CNS and thymus of treated animals. These studies suggest that oxidative stress mediates ts1-induced neurodegeneration and T-cell loss.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.