ReviewACS omega2024
Glutathione Depletion and Stalwart Anticancer Activity of Metallotherapeutics Inducing Programmed Cell Death: Opening a New Window for Cancer Therapy.
Review in ACS omega, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed.
- Quercetin-Driven Redox Sensitization Enhances the Antitumor Activity of a Thiol-Reactive Agent through Glutathione Disruption.ACS omega · 2026Article
- FeiScience · 2026Article
- Article
- Article
- Glutathione in Our Diet and Its Role in the Body: From Disease Prevention to Anti-Aging.Nutrients · 2026Review
- Review
- Self-synergizing mutual prodrug liposomes for targeted cancer therapyTheranostics · 2026Article
- Targeted phytotherapy: essential oils, multi-target cancer action & nanodelivery.Frontiers in oncology · 2026Review
- Improved Physicochemical Stability and Retinoblastoma Anticancer Activity of Salt-Caged Acid-Base Neutralized Melphalan Loaded in L-Glutathione and pH Responsive Fattigated Nanoparticles.International journal of nanomedicine · 2026Article
- Atovaquone-induced oxidative stress activates the pentose phosphate pathway and Immunogenic cell death in ovarian cancer.Scientific reports · 2025Article
- Strategies for enhancing the adaptive response to oxidative stress in microbial cell factories.World journal of microbiology & biotechnology · 2025Review
- Review
- Nanotherapeutics induced redox resetting of oxidative and nitrosative stress: targeting glutathione-depletion in cancer.Nanomedicine (London, England) · 2025Review
- Nanocarriers for cutting-edge cancer immunotherapies.Journal of translational medicine · 2025Review
- Absorptivity Is an Important Determinant in the Toxicity Difference between Aristolochic Acid I and Aristolochic Acid II.Journal of agricultural and food chemistry · 2025Article
- Harnessing the interaction between redox signaling and senescence to restrain tumor drug resistance.Frontiers in cell and developmental biology · 2025Review
- The outcast of medicine: metals in medicine--from traditional mineral medicine to metallodrugs.Frontiers in pharmacology · 2025Review
- The role of cytostatic in oxidative stress reactions.Frontiers in oncology · 2025Review
- Reactive Oxygen Species-Sensitive Nanophotosensitizers Composed of Buthionine Sulfoximine-Conjugated Chitosan Oligosaccharide for Enhanced Photodynamic Treatment of Cancer Cells.International journal of molecular sciences · 2024Article
- Inorganic Nanomedicine-Mediated Ferroptosis: A Synergistic Approach to Combined Cancer Therapies and Immunotherapy.Cancers · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cellular defense system against exogenous substances makes therapeutics inefficient as intracellular glutathione (GSH) exhibits an astounding antioxidant activity in scavenging reactive oxygen species (ROS) or reactive nitrogen species (RNS) or other free radicals produced by the therapeutics. In the cancer cell microenvironment, the intracellular GSH level becomes exceptionally high to fight against oxidative stress created by the production of ROS/RNS or any free radicals, which are the byproducts of intracellular redox reactions or cellular respiration processes. Thus, in order to maintain redox homeostasis for survival of cancer cells and their rapid proliferation, the GSH level starts to escalate. In this circumstance, the administration of anticancer therapeutics is in vain, as the elevated GSH level reduces their potential by reduction or by scavenging the ROS/RNS they produce. Therefore, in order to augment the therapeutic potential of anticancer agents against elevated GSH condition, the GSH level must be depleted by hook or by crook. Hence, this Review aims to compile precisely the role of GSH in cancer cells, the importance of its depletion for cancer therapy and examples of anticancer activity of a few selected metal complexes which are able to trigger cancer cell death by depleting the GSH level.
Identifiers
What OpenQuestion holds
Registered trials
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.