ArticleCancer letters2015
Superoxide induces protein oxidation in plasma and TNF-α elevation in macrophage culture: Insights into mechanisms of neurotoxicity following doxorubicin chemotherapy.
Article in Cancer letters, 2015. 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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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.
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Who cites it
22 citing papers in PubMed, 45 citations in OpenAlex.
- Mechanistic insights and therapeutic interventions of mitochondrial quality control in chemotherapy-related cognitive impairment.Neoplasia (New York, N.Y.) · 2026Review
- Different Mechanisms in Doxorubicin-Induced Neurotoxicity: Impact of BRCA Mutations.International journal of molecular sciences · 2025Review
- Inhibition of intracellular versus extracellular cathepsin D differentially alters the liver lipidome of mice with metabolic dysfunction-associated steatohepatitis.The FEBS journal · 2025Article
- Synergistic anti-cancer effects of piezoelectric hexagonal boron nitride nanocarriers for controlled doxorubicin release.Nanomedicine (London, England) · 2025Article
- GABA Administration Ameliorates the Toxicity of Doxorubicin on CSF and the Brain of Albino Rats.Annals of neurosciences · 2024Article
- Treadmill exercise ameliorates chemotherapy-induced memory impairment through Wnt/β-catenin signaling pathway.Journal of exercise rehabilitation · 2023Article
- Piracetam as a Therapeutic Agent for Doxorubicin-Induced Cognitive Deficits by Enhancing Cholinergic Functions and Reducing Neuronal Inflammation, Apoptosis, and Oxidative Stress in Rats.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Antioxidant and Antimicrobial Peptides Derived from Food Proteins.Molecules (Basel, Switzerland) · 2022Review
- Galectin-1 Cooperates with Yersinia Outer Protein (Yop) P to Thwart Protective Immunity by Repressing Nitric Oxide Production.Biomolecules · 2021Article
- Chemotherapy-induced cognitive impairment: focus on the intersection of oxidative stress and TNFα.Cellular and molecular life sciences : CMLS · 2021Review
- Neuroprotective Potential of Ellagic Acid: A Critical Review.Advances in nutrition (Bethesda, Md.) · 2021Review
- Oxidative Stress and Cognitive Alterations Induced by Cancer Chemotherapy Drugs: A Scoping Review.Antioxidants (Basel, Switzerland) · 2021Article
- Inadvertent intrathecal administration of daunomycin resulting in fatality: Case report and therapeutic considerations.eNeurologicalSci · 2021Article
- The effect of oleuropein on unilateral ureteral obstruction induced-kidney injury in rats: the role of oxidative stress, inflammation and apoptosis.Molecular biology reports · 2020Article
- Plausible biochemical mechanisms of chemotherapy-induced cognitive impairment ("chemobrain"), a condition that significantly impairs the quality of life of many cancer survivors.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Article
- CCancer nanotechnology · 2018Article
- Neuroprotective Effects of dl-3-n-Butylphthalide against Doxorubicin-Induced Neuroinflammation, Oxidative Stress, Endoplasmic Reticulum Stress, and Behavioral Changes.Oxidative medicine and cellular longevity · 2018Article
- Acute treatment with doxorubicin affects glutamate neurotransmission in the mouse frontal cortex and hippocampus.Brain research · 2017Article
- Effect of oleuropein against chemotherapy drug-induced histological changes, oxidative stress, and DNA damages in rat kidney injury.Journal of food and drug analysis · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Chemotherapy-induced cognitive impairment (CICI) is a quality of life-altering consequence of chemotherapy experienced by a large percentage of cancer survivors. Approximately half of FDA-approved anti-cancer drugs are known to produce ROS. Doxorubicin (Dox), a prototypical ROS-generating chemotherapeutic agent, generates superoxide (O2(-)•) via redox cycling. Our group previously demonstrated that Dox, which does not cross the BBB, induced oxidative damage to plasma proteins leading to TNF-α elevation in the periphery and, subsequently, in brain following cancer chemotherapy. We hypothesize that such processes play a central role in CICI. The current study tested the notion that O2(-)• is involved and likely responsible for Dox-induced plasma protein oxidation and TNF-α release. Addition of O2(-)• as the potassium salt (KO2) to plasma resulted in significantly increased oxidative damage to proteins, indexed by protein carbonyl (PC) and protein-bound HNE levels. We then adapted this protocol for use in cell culture. Incubation of J774A.1 macrophage culture using this KO2-18crown6 protocol with 1 and 10 µM KO2 resulted in dramatically increased levels of TNF-α produced. These findings, together with our prior results, provide strong evidence that O2(-)• and its resulting reactive species are critically involved in Dox-induced plasma protein oxidation and TNF-α release.
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