Measuring Glutathione Redox Potential of HIV-1-infected Macrophages

Bhaskar, Ashima; Munshi, MohamedHusen; Khan, Sohrab; Fatima, Sadaf; Arya, Rahul; Jameel, Shahid; Singh, Amit

doi:10.1074/jbc.m114.588913

Cited by 62 publications

(117 citation statements)

References 83 publications

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“…MBB reacts nonenzymatically with GSH and binds to thiol groups, and it is excited by UV light and then emits bluish fluorescence at 450 nm with an intensity that is proportional to the intracellular GSH content (35,36). GSH and GSSG levels were also measured using a glutathione assay kit as per the manufacturer's instructions (37). Briefly, 2 ϫ 10 7 cells from various experiments were collected in 500 l of cold 50 M MES buffer and sonicated.…”

Section: Methodsmentioning

confidence: 99%

myo-Inositol Oxygenase Overexpression Accentuates Generation of Reactive Oxygen Species and Exacerbates Cellular Injury following High Glucose Ambience

Sun

Dutta

Xie

et al. 2016

Journal of Biological Chemistry

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increased ROS generation, depleted reduced glutathione, reduced GSH/GSSG ratio, and enhanced adaptive changes in the profile of the antioxidant defense system. These changes were also accompanied by mitochondrial dysfunctions, DNA damage and induction of apoptosis, accentuated activity of profibrogenic cytokine, and expression of fibronectin, the latter two being the major hallmarks of DN. These perturbations were largely blocked by various ROS inhibitors (Mito Q, diphenyleneiodonium chloride, and N-acetylcysteine) and MIOX/NOX4 siRNA. In conclusion, this study highlights a novel mechanism where MIOX under HG ambience exacerbates renal injury during the progression of diabetic nephropathy following the generation of excessive ROS via an unexplored G-X pathway.

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Section: Methodsmentioning

confidence: 99%

myo-Inositol Oxygenase Overexpression Accentuates Generation of Reactive Oxygen Species and Exacerbates Cellular Injury following High Glucose Ambience

Sun

Dutta

Xie

et al. 2016

Journal of Biological Chemistry

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“…4,5 Using a mitochondria-specific roGFP, Bhaskar et al showed that the values of E GSH are similar in the cytosol and mitochondria (~ −310 mV). 6 However, this measurement approached the detection limit of roGFP, which may underestimate the mGSH level. Additionally, E GSH is proportional to [GSH] 2 :[GSSG].…”

mentioning

confidence: 90%

Reversible Reaction-Based Fluorescent Probe for Real-Time Imaging of Glutathione Dynamics in Mitochondria

et al. 2017

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We report a mitochondria-specific glutathione (GSH) probe—designated as Mito-RealThiol (MitoRT)—that can monitor in vivo real-time mitochondrial glutathione dynamics, and apply this probe to follow mitochondrial GSH dynamic changes in living cells for the first time. MitoRT can be utilized in confocal microscopy, super-resolution fluorescence imaging, and flow cytometry systems. Using MitoRT, we demonstrate that cells have a high priority to maintain the GSH level in mitochondria compared to the cytosol not only under normal growing conditions but also upon oxidative stress.

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“…Interestingly, transcription activation by exogenous hydrogen peroxide takes place only after the prolonged treatment, allowing us to hypothesize that virus-induced oxidative stress can play a crucial role in activation of the latent viral infection [138]. Supporting this, activation of the latent infection was triggered by modest changes in the cell redox potential (25 mV) [144]. Such changes can be induced either directly by HIV proteins or indirectly through the induction of proinflammatory cytokines such as TNF- α [145].…”

Section: Ros In Hiv's Life Cyclementioning

confidence: 99%

Oxidative Stress during HIV Infection: Mechanisms and Consequences

Ivanov

Valuev-Elliston

Иванова

et al. 2016

Oxidative Medicine and Cellular Longevity

291

246

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It is generally acknowledged that reactive oxygen species (ROS) play crucial roles in a variety of natural processes in cells. If increased to levels which cannot be neutralized by the defense mechanisms, they damage biological molecules, alter their functions, and also act as signaling molecules thus generating a spectrum of pathologies. In this review, we summarize current data on oxidative stress markers associated with human immunodeficiency virus type-1 (HIV-1) infection, analyze mechanisms by which this virus triggers massive ROS production, and describe the status of various defense mechanisms of the infected host cell. In addition, we have scrutinized scarce data on the effect of ROS on HIV-1 replication. Finally, we present current state of knowledge on the redox alterations as crucial factors of HIV-1 pathogenicity, such as neurotoxicity and dementia, exhaustion of CD4+/CD8+ T-cells, predisposition to lung infections, and certain side effects of the antiretroviral therapy, and compare them to the pathologies associated with the nitrosative stress.

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Measuring Glutathione Redox Potential of HIV-1-infected Macrophages

Cited by 62 publications

References 83 publications

myo-Inositol Oxygenase Overexpression Accentuates Generation of Reactive Oxygen Species and Exacerbates Cellular Injury following High Glucose Ambience

myo-Inositol Oxygenase Overexpression Accentuates Generation of Reactive Oxygen Species and Exacerbates Cellular Injury following High Glucose Ambience

Reversible Reaction-Based Fluorescent Probe for Real-Time Imaging of Glutathione Dynamics in Mitochondria

Oxidative Stress during HIV Infection: Mechanisms and Consequences

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