ArticleJournal of bioenergetics and biomembranes2010
Brain mitochondria from rats treated with sulforaphane are resistant to redox-regulated permeability transition.
Article in Journal of bioenergetics and biomembranes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 63 citations in OpenAlex.
- Nrf2 modulates cytosolic and mitochondrial calcium signal.Redox biology · 2026Article
- FoxO3a: capture the bond between magnesium and diabetic kidney disease.Frontiers in endocrinology · 2025Review
- Molecular mechanisms of sulforaphane in Alzheimer's disease: insights from an in-silico study.In silico pharmacology · 2024Article
- The Interplay between Mitochondrial Dysfunction and Ferroptosis during Ischemia-Associated Central Nervous System Diseases.Brain sciences · 2023Review
- The crosstalk between ferroptosis and mitochondrial dynamic regulatory networks.International journal of biological sciences · 2023Review
- Long-term sulforaphane-treatment restores redox homeostasis and prevents cognitive decline in middleaged female and male rats, but cannot revert previous damage in old animals.Biogerontology · 2022Article
- Review
- The role of nutrients in human neurodevelopment and their potential to prevent neurodevelopmental adversity.Frontiers in nutrition · 2022Review
- Article
- Beneficial effects of δ-tocotrienol against oxidative stress in osteoblastic cells: studies on the mechanisms of action.European journal of nutrition · 2020Article
- Transcriptional activation of antioxidant gene expression by Nrf2 protects against mitochondrial dysfunction and neuronal death associated with acute and chronic neurodegeneration.Experimental neurology · 2020Review
- The role of Nrf2 signaling in counteracting neurodegenerative diseases.The FEBS journal · 2018Review
- Targeting Nrf2 to Suppress Ferroptosis and Mitochondrial Dysfunction in Neurodegeneration.Frontiers in neuroscience · 2018Review
- Nrf2, the Master Regulator of Anti-Oxidative Responses.International journal of molecular sciences · 2017Review
- The multifaceted role of Nrf2 in mitochondrial function.Current opinion in toxicology · 2016Review
- The emerging role of Nrf2 in mitochondrial function.Free radical biology & medicine · 2015Review
- Resveratrol Preconditioning Protects Against Cerebral Ischemic Injury via Nuclear Erythroid 2-Related Factor 2.Stroke · 2015Article
- Permeability transition pore-dependent and PARP-mediated depletion of neuronal pyridine nucleotides during anoxia and glucose deprivation.Journal of bioenergetics and biomembranes · 2015Article
- Nrf2-ARE activator carnosic acid decreases mitochondrial dysfunction, oxidative damage and neuronal cytoskeletal degradation following traumatic brain injury in mice.Experimental neurology · 2015Article
- Neuroprotective Effect of Brassica oleracea Sprouts Crude Juice in a Cellular Model of Alzheimer's Disease.Oxidative medicine and cellular longevity · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress promotes Ca2+-dependent opening of the mitochondrial inner membrane permeability transition pore (PTP), causing bioenergetic failure and subsequent cell death in many paradigms, including those related to acute brain injury. One approach to pre-conditioning against oxidative stress is pharmacologic activation of the Nrf2/ARE pathway of antioxidant gene expression by agents such as sulforaphane (SFP). This study tested the hypothesis that administration of SFP to normal rats increases resistance of isolated brain mitochondria to redox-sensitive PTP opening. SFP or DMSO vehicle was administered intraperitoneally to adult male rats at 10 mg/kg 40 h prior to isolation of non-synaptic brain mitochondria. Mitochondria were suspended in medium containing a respiratory substrate and were exposed to an addition of Ca2+ below the threshold for PTP opening. Subsequent addition of tert-butyl hydroperoxide (tBOOH) resulted in a cyclosporin A-inhibitable release of accumulated Ca2+ into the medium, as monitored by an increase in fluorescence of Calcium Green 5N within the medium, and was preceded by a decrease in the autofluorescence of mitochondrial NAD(P)H. SFP treatment significantly reduced the rate of tBOOH-induced Ca2+ release but did not affect NAD(P)H oxidation or inhibit PTP opening induced by the addition of phenylarsine oxide, a direct sulfhydryl oxidizing agent. SFP treatment had no effect on respiration by brain mitochondria and had no effect on PTP opening or respiration when added directly to isolated mitochondria. We conclude that SFP confers resistance of brain mitochondria to redox-regulated PTP opening, which could contribute to neuroprotection observed with SFP.
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