ArticleIranian journal of pharmaceutical research : IJPR2013
Mitochondrial toxicity of depleted uranium: protection by Beta-glucan.
Article in Iranian journal of pharmaceutical research : IJPR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
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- Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria.International journal of molecular sciences · 2023Review
- Adverse effect propensity: A new feature of Gulf War illness predicted by environmental exposures.iScience · 2023Article
- Review of Knowledge of Uranium-Induced Kidney Toxicity for the Development of an Adverse Outcome Pathway to Renal Impairment.International journal of molecular sciences · 2022Review
- Pyrroloquinoline quinone alleviates oxidative damage induced by high glucose in HepG2 cells.Saudi journal of biological sciences · 2021Article
- Zinc and selenium supplement mitigated valproic acid-induced testis toxicity by modulating the oxidative redox balance in male rats.Anatomy & cell biology · 2021Article
- β-Glucans as Dietary Supplement to Improve Locomotion and Mitochondrial Respiration in a Model of Duchenne Muscular Dystrophy.Nutrients · 2021Article
- A Review on Toxicodynamics of Depleted Uranium.Iranian journal of pharmaceutical research : IJPR · 2019Review
- The toxicological mechanisms and detoxification of depleted uranium exposure.Environmental health and preventive medicine · 2018Review
- Embryo-Protective Effects of Cerium Oxide Nanoparticles against Gestational Diabetes in Mice.Iranian journal of pharmaceutical research : IJPR · 2018Article
- Atorvastatin attenuates ethanol-induced hepatotoxicity via antioxidant and anti-inflammatory mechanisms.Research in pharmaceutical sciences · 2017Article
- The effect of epicatechin on oxidative stress and mitochondrial damage induced by homocycteine using isolated rat hippocampus mitochondria.Research in pharmaceutical sciences · 2017Article
- Nanoceria Attenuated High Glucose-Induced Oxidative Damage in HepG2 Cells.Cell journal · 2016Article
- Hepatic transcriptomic profiling reveals early toxicological mechanisms of uranium in Atlantic salmon (Salmo salar).BMC genomics · 2014Article
- Schizophrenia induces oxidative stress and cytochrome C release in isolated rat brain mitochondria: a possible pathway for induction of apoptosis and neurodegeneration.Iranian journal of pharmaceutical research : IJPR · 2014Article
- Toxicity of Arsenic (III) on Isolated Liver Mitochondria: A New Mechanistic Approach.Iranian journal of pharmaceutical research : IJPR · 2013Article
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Considerable evidence suggests that mitochondrial dysfunction contributes to the toxicity of uranyl acetate (UA), a soluble salt of depleted uranium (DU). We examined the ability of the two antioxidants, beta-glucan and butylated hydroxyl toluene (BHT), to prevent UA-induced mitochondrial dysfunction using rat-isolated kidney mitochondria. Beta-glucan (150 nM) and BHT (20 nM) attenuated UA-induced mitochondrial reactive oxygen species (ROS) formation, lipid peroxidation and glutathione oxidation. Beta-glucan and BHT also prevented the loss of mitochondrial membrane potential (MMP) and mitochondrial swelling following the UA treatment in isolated mitochondria. Our results show that beta-glucan and BHT prevented UA-induced mitochondrial outer membrane damage as well as release of cytochrome c from mitochondria. UA also decreased the ATP production in isolated mitochondria significantly inhibited with beta-glucan and BHT pre-treatment. Our results showed that beta-glucan may be mitochondria-targeted antioxidant and suggested this compound as a possible drug candidate for prophylaxis and treatment against DU-induced nephrotoxicity.
Indexed as
Identifiers
24250581PMC3813223W2135330163What 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.