ArticleNeurotoxicity research2012
Acute brain damage induced by acetaminophen in mice: effect of diphenyl diselenide on oxidative stress and mitochondrial dysfunction.
Article in Neurotoxicity research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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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
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Evaluation of the evidence on acetaminophen use and neurodevelopmental disorders using the Navigation Guide methodology.Environmental health : a global access science source · 2025Pooled it
- The possible effect of coenzyme Q10 and captopril on acetaminophen-induced encephalopathy in rats: possible influence on autophagy, antioxidant and NaArchives of medical science : AMS · 2025Article
- Elderly mice with history of acetaminophen intoxication display worsened cognitive impairment and persistent elevation of astrocyte and microglia burden.Scientific reports · 2024Article
- Diphenyl Diselenide Attenuates Mitochondrial Damage During Initial Hypoxia and Enhances Resistance to Recurrent Hypoxia.Neurotoxicity research · 2024Article
- Article
- Potential adverse actions of prenatal exposure of acetaminophen to offspring.Frontiers in pharmacology · 2023Review
- Paracetamol (Acetaminophen) and its Effect on the Developing Mouse Brain.Frontiers in toxicology · 2022Article
- Toxicology and pharmacology of synthetic organoselenium compounds: an update.Archives of toxicology · 2021Review
- Association of Prenatal Acetaminophen Exposure Measured in Meconium With Risk of Attention-Deficit/Hyperactivity Disorder Mediated by Frontoparietal Network Brain Connectivity.JAMA pediatrics · 2020Observational
- Effects of caffeine on brain antioxidant status and mitochondrial respiration in acetaminophen-intoxicated mice.Toxicology research · 2020Article
- N-acetyl cysteine treatment preserves mitochondrial indices of functionality in the brain of hyperammonemic mice.Clinical and experimental hepatology · 2020Article
- Comparison of effects of high and low dose paracetamol treatment and toxicity on brain and liver in rats.Northern clinics of Istanbul · 2020Article
- Acetaminophen Intoxication Rapidly Induces Apoptosis of Intestinal Crypt Stem Cells and Enhances Intestinal Permeability.Hepatology communications · 2019Article
- Antibacterial and antioxidant effects ofJournal of traditional and complementary medicine · 2019Article
- The potential role of mitochondrial impairment in the pathogenesis of imatinib-induced renal injury.Heliyon · 2019Article
- Taurine supplementation abates cirrhosis-associated locomotor dysfunction.Clinical and experimental hepatology · 2018Article
- Extrahepatic toxicity of acetaminophen: critical evaluation of the evidence and proposed mechanisms.Journal of clinical and translational research · 2018Review
- Acetaminophen from liver to brain: New insights into drug pharmacological action and toxicity.Pharmacological research · 2016Review
- Atrasentan increased the expression of klotho by mediating miR-199b-5p and prevented renal tubular injury in diabetic nephropathy.Scientific reports · 2016Article
- Effects of organoselenium compounds on early and late brain biochemical alterations in sepsis-survivor rats.Neurotoxicity research · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Organoselenium compounds exhibit antioxidant activity, as well as a variety of biological activities, with potential pharmacological and therapeutic applications. The aim of this study was to investigate the effect of diphenyl diselenide (PhSe)(2) in reversing oxidative brain damage and mitochondrial dysfunction caused by administration of acetaminophen (APAP) in mice. Mice received a toxic dose of APAP, followed by a dose of (PhSe)(2) 1 h later. Four hours after the administration of APAP, plasma was withdrawn from the mice and used for biochemical assays of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) as markers of hepatotoxicity. Brain homogenate was examined to determine oxidative stress. Isolated brain mitochondria were examined to quantify mitochondrial transmembrane's electrical potential and mitochondrial swelling and to estimate reactive oxygen species (ROS) production. APAP administration caused an increase in plasma ALT and AST activities. APAP administration also caused a significant increase in the levels of thiobarbituric acid reactive substances (TBARS) and dichlorofluorescein oxidation in brain homogenate. Similarly, mitochondrial swelling and ROS production increased after APAP administration. APAP treatment also caused a decrease in Na(+), K(+)- ATPase activity and in mitochondrial membrane potential. These alterations observed in the brain of APAP-treated mice were restored by (PhSe)(2). Glutathione levels were decreased by APAP, but (PhSe)(2) did not reverse this change. Treatment with (PhSe)(2) after APAP administration can reverse the neurotoxicity caused by a single toxic dose of APAP. The neuroprotective effect of (PhSe)(2) is likely associated with its antioxidant properties.
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Registered trials
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