ArticleExperimental neurology2014
N-acetylcysteine amide preserves mitochondrial bioenergetics and improves functional recovery following spinal trauma.
Article in Experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 106 citations in OpenAlex.
- Neural correlates of clinical improvement in response to N-acetylcysteine in adolescents with non-suicidal self-injury.Progress in neuro-psychopharmacology & biological psychiatry · 2020Trial
- Proteomics reveal PTEN as a critical mediator of sustained mitochondrial dysfunction during chronic spinal cord injury.Experimental neurology · 2026Article
- N-acetyl cysteine amide mitigates oxidative stress and apoptosis in a rat model of renal ischemia-reperfusion injury.Scientific reports · 2026Article
- N-Acetylcysteine Amide Is a Potential Novel Radioprotector of Salivary Gland Function.Cancers · 2025Article
- Mitochondrial Complex I and ROS control neuromuscular function through opposing pre- and postsynaptic mechanisms.PLoS biology · 2025Article
- Mitochondrial Complex I and ROS control neuromuscular function through opposing pre- and postsynaptic mechanisms.bioRxiv : the preprint server for biology · 2025Article
- Traumatic spinal cord injury: a review of the current state of art and future directions - what do we know and where are we going?North American Spine Society journal · 2025Article
- Advancements in Antioxidant-Based Therapeutics for Spinal Cord Injury: A Critical Review of Strategies and Combination Approaches.Antioxidants (Basel, Switzerland) · 2024Review
- Microglia-induced neuroinflammation in hippocampal neurogenesis following traumatic brain injury.Heliyon · 2024Review
- The Effect of Glycine and N-Acetylcysteine on Oxidative Stress in the Spinal Cord and Skeletal Muscle After Spinal Cord Injury.Inflammation · 2024Article
- Investigating LIM (Lin-11, Isl-1, and Mec-3) Kinases and Their Correlation with Pathological Events and Microtubule Dynamics in an Experimental Model of Spinal Cord Injury in Rats.ACS pharmacology & translational science · 2024Article
- Mitochondria-Targeted Antioxidant Therapeutics for Traumatic Brain Injury.Antioxidants (Basel, Switzerland) · 2024Review
- Article
- Treatment effects of N-acetyl cysteine on resting-state functional MRI and cognitive performance in patients with chronic mild traumatic brain injury: a longitudinal study.Frontiers in neurology · 2024Article
- Data and subject heterogeneity and data sharing: keys to translational success in spinal cord injury research?Neural regeneration research · 2023Article
- N-acetylcysteine Pharmacology and Applications in Rare Diseases-Repurposing an Old Antioxidant.Antioxidants (Basel, Switzerland) · 2023Review
- Mitochondria dysfunction and bipolar disorder: From pathology to therapy.IBRO neuroscience reports · 2023Article
- Delivery of mitoceuticals or respiratory competent mitochondria to sites of neurotrauma.Mitochondrion · 2023Review
- Platelet mitochondria, a potent immune mediator in neurological diseases.Frontiers in physiology · 2023Review
- Pioglitazone restores mitochondrial function but does not spare cortical tissue following mild brain contusion.Brain communications · 2023Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Mitochondrial dysfunction is becoming a pivotal target for neuroprotective strategies following contusion spinal cord injury (SCI) and the pharmacological compounds that maintain mitochondrial function confer neuroprotection and improve long-term hindlimb function after injury. In the current study we evaluated the efficacy of cell-permeating thiol, N-acetylcysteine amide (NACA), a precursor of endogenous antioxidant glutathione (GSH), on mitochondrial function acutely, and long-term tissue sparing and hindlimb locomotor recovery following upper lumbar contusion SCI. Some designated injured adult female Sprague-Dawley rats (n=120) received either vehicle or NACA (75, 150, 300 or 600mg/kg) at 15min and 6h post-injury. After 24h the total, synaptic, and non-synaptic mitochondrial populations were isolated from a single 1.5cm spinal cord segment (centered at injury site) and assessed for mitochondrial bioenergetics. Results showed compromised total mitochondrial bioenergetics following acute SCI that was significantly improved with NACA treatment in a dose-dependent manner, with maximum effects at 300mg/kg (n=4/group). For synaptic and non-synaptic mitochondria, only 300mg/kg NACA dosage showed efficacy. Similar dosage (300mg/kg) also maintained mitochondrial GSH near normal levels. Other designated injured rats (n=21) received continuous NACA (150 or 300mg/kg/day) treatment starting at 15min post-injury for one week to assess long-term functional recovery over 6weeks post-injury. Locomotor testing and novel gait analyses showed significantly improved hindlimb function with NACA that were associated with increased tissue sparing at the injury site. Overall, NACA treatment significantly maintained acute mitochondrial bioenergetics and normalized GSH levels following SCI, and prolonged delivery resulted in significant tissue sparing and improved recovery of hindlimb function.
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