ArticleThe Journal of pharmacology and experimental therapeutics2012
γ-Tocotrienol protects against mitochondrial dysfunction and renal cell death.
Article in The Journal of pharmacology and experimental therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Mitochondrial dysfunction as a key player in aggravating periodontitis among diabetic patients: review of the current scope of knowledge.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Gamma-tocopherol vitamin E enhances the cytotoxicity of p-cresyl sulfate to renal tubular cells.European journal of medical research · 2025Article
- Tocotrienols Provide Radioprotection to Multiple Organ Systems through Complementary Mechanisms of Antioxidant and Signaling Effects.Antioxidants (Basel, Switzerland) · 2023Review
- Effects of Gamma-Tocotrienol on Partial-Body Irradiation-Induced Intestinal Injury in a Nonhuman Primate Model.Antioxidants (Basel, Switzerland) · 2022Article
- γ-Tocotrienol Protects against Mitochondrial Dysfunction, Energy Deficits, Morphological Damage, and Decreases in Renal Functions after Renal Ischemia.International journal of molecular sciences · 2021Article
- Mitigation of late cardiovascular effects of oxygen ion radiation by γ-tocotrienol in a mouse model.Life sciences in space research · 2021Article
- Utilization of Vitamin E Analogs to Protect Normal Tissues While Enhancing Antitumor Effects.Seminars in radiation oncology · 2019Review
- Tocotrienol-Rich Fraction of Palm Oil Improves Behavioral Impairments and Regulates Metabolic Pathways in AβPP/PS1 Mice.Journal of Alzheimer's disease : JAD · 2018Article
- Cytoresistance after acute kidney injury is limited to the recovery period of proximal tubule integrity and possibly involves Hippo-YAP signaling.Physiological reports · 2017Article
- Tocotrienol-Rich Fraction Ameliorates Antioxidant Defense Mechanisms and Improves Replicative Senescence-Associated Oxidative Stress in Human Myoblasts.Oxidative medicine and cellular longevity · 2017Article
- Article
- The Vitamin E Analog Gamma-Tocotrienol (GT3) Suppresses Radiation-Induced Cytogenetic Damage.Pharmaceutical research · 2016Article
- γ-Tocotrienol as a Promising Countermeasure for Acute Radiation Syndrome: Current Status.International journal of molecular sciences · 2016Review
- Article
- A tocotrienol-enriched formulation protects against radiation-induced changes in cardiac mitochondria without modifying late cardiac function or structure.Radiation research · 2015Article
- Dietary Tocotrienol/γ-Cyclodextrin Complex Increases Mitochondrial Membrane Potential and ATP Concentrations in the Brains of Aged Mice.Oxidative medicine and cellular longevity · 2015Article
- Molecular dynamics guided design of tocoflexol: a new radioprotectant tocotrienol with enhanced bioavailability.Drug development research · 2014Article
- Pharmacological potential of tocotrienols: a review.Nutrition & metabolism · 2014Review
- Protein kinase C-α interaction with iHSP70 in mitochondria promotes recovery of mitochondrial function after injury in renal proximal tubular cells.American journal of physiology. Renal physiology · 2013Article
- Development and validation of a sensitive LC/MS/MS method for the determination of γ-tocotrienol in rat plasma: application to pharmacokinetic studies.Biomedical chromatography : BMC · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress is a major mechanism of a variety of renal diseases. Tocopherols and tocotrienols are well known antioxidants. This study aimed to determine whether γ-tocotrienol (GT3) protects against mitochondrial dysfunction and renal proximal tubular cell (RPTC) injury caused by oxidants. Primary cultures of RPTCs were injured by using tert-butyl hydroperoxide (TBHP) in the absence and presence of GT3 or α-tocopherol (AT). Reactive oxygen species (ROS) production increased 300% in TBHP-injured RPTCs. State 3 respiration, oligomycin-sensitive respiration, and respiratory control ratio (RCR) decreased 50, 63, and 47%, respectively. The number of RPTCs with polarized mitochondria decreased 54%. F₀F₁-ATPase activity and ATP content decreased 31 and 65%, respectively. Cell lysis increased from 3% in controls to 26 and 52% at 4 and 24 h, respectively, after TBHP exposure. GT3 blocked ROS production, ameliorated decreases in state 3 and oligomycin-sensitive respirations and F₀F₁-ATPase activity, and maintained RCR and mitochondrial membrane potential (ΔΨ(m)) in injured RPTCs. GT3 maintained ATP content, blocked RPTC lysis at 4 h, and reduced it to 13% at 24 h after injury. Treatment with equivalent concentrations of AT did not block ROS production and cell lysis and moderately improved mitochondrial respiration and coupling. This is the first report demonstrating the protective effects of GT3 against RPTC injury by: 1) decreasing production of ROS, 2) improving mitochondrial respiration, coupling, ΔΨ(m), and F₀F₁-ATPase function, 3) maintaining ATP levels, and 4) preventing RPTC lysis. Our data suggest that GT3 is superior to AT in protecting RPTCs against oxidant injury and may prove therapeutically valuable for preventing renal injury associated with oxidative stress.
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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.