ArticleNeurobiology of disease2014
Nicotinamide pre-treatment ameliorates NAD(H) hyperoxidation and improves neuronal function after severe hypoxia.
Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- PARP inhibitors target cellular energy metabolism: Mechanisms of action and clinical implications.Translational oncology · 2026Review
- Nicotinamide counteracts Rotenone-induced mitochondrial and neuronal dysfunction in a translational early-life model.Scientific reports · 2026Article
- The effect of mephedrone on human neuroblastoma and astrocytoma cells.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Article
- Role of NADCellular and molecular neurobiology · 2023Review
- Conformational Preferences of Pyridone Adenine Dinucleotides from Molecular Dynamics Simulations.International journal of molecular sciences · 2022Article
- Interactive Effects of Swimming High-Intensity Interval Training and Resveratrol Supplementation Improve Mitochondrial Protein Levels in the Hippocampus of Aged Rats.BioMed research international · 2022Article
- Brain tissue oxygen dynamics while mimicking the functional deficiency of interneurons.Frontiers in cellular neuroscience · 2022Article
- Early Development of the GABAergic System and the Associated Risks of Neonatal Anesthesia.International journal of molecular sciences · 2021Review
- Contrasting Metabolic Insufficiency in Aging and Dementia.Aging and disease · 2021Review
- Role of apoptosis-inducing factor in perinatal hypoxic-ischemic brain injury.Neural regeneration research · 2021Review
- The Contribution of Dysfunctional Chloride Channels to Neurovascular Deficiency and Neurodegeneration.Frontiers in pharmacology · 2021Article
- B Vitamins and Fatty Acids: What Do They Share with Small Vessel Disease-Related Dementia?International journal of molecular sciences · 2019Review
- Niacin in the Central Nervous System: An Update of Biological Aspects and Clinical Applications.International journal of molecular sciences · 2019Review
- Age- and AD-related redox state of NADH in subcellular compartments by fluorescence lifetime imaging microscopy.GeroScience · 2019Article
- Role of Nicotinamide Adenine Dinucleotide and Related Precursors as Therapeutic Targets for Age-Related Degenerative Diseases: Rationale, Biochemistry, Pharmacokinetics, and Outcomes.Antioxidants & redox signaling · 2019Review
- The Influence of Nicotinamide on Health and Disease in the Central Nervous System.International journal of tryptophan research : IJTR · 2018Review
- Longitudinal in vivo tracking of adverse effects following topical steroid treatment.Experimental dermatology · 2016Article
- Enhancing Nervous System Recovery through Neurobiologics, Neural Interface Training, and Neurorehabilitation.Frontiers in neuroscience · 2016Review
- Metabolic responses differentiate between interictal, ictal and persistent epileptiform activity in intact, immature hippocampus in vitro.Neurobiology of disease · 2015Article
- Nicotinamide improves sevoflurane-induced cognitive impairment through suppression of inflammation and anti-apoptosis in rat.International journal of clinical and experimental medicine · 2015Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Prolonged hypoxia leads to irreversible loss of neuronal function and metabolic impairment of nicotinamide adenine dinucleotide recycling (between NAD(+) and NADH) immediately after reoxygenation, resulting in NADH hyperoxidation. We test whether the addition of nicotinamide (to enhance NAD(+) levels) or PARP-1 inhibition (to prevent consumption of NAD(+)) can be effective in improving either loss of neuronal function or hyperoxidation following severe hypoxic injury in hippocampal slices. After severe, prolonged hypoxia (maintained for 3min after spreading depression) there was hyperoxidation of NADH following reoxygenation, an increased soluble NAD(+)/NADH ratio, loss of neuronal field excitatory post-synaptic potential (fEPSP) and decreased ATP content. Nicotinamide incubation (5mM) 2h prior to hypoxia significantly increased total NAD(H) content, improved neuronal recovery, enhanced ATP content, and prevented NADH hyperoxidation. The nicotinamide-induced increase in total soluble NAD(H) was more significant in the cytosolic compartment than within mitochondria. Prolonged incubation with PJ-34 (>1h) led to enhanced baseline NADH fluorescence prior to hypoxia, as well as improved neuronal recovery, NADH hyperoxidation and ATP content on recovery from severe hypoxia and reoxygenation. In this acute model of severe neuronal dysfunction prolonged incubation with either nicotinamide or PJ-34 prior to hypoxia improved recovery of neuronal function, enhanced NADH reduction and ATP content, but neither treatment restored function when administered during or after prolonged hypoxia and reoxygenation.
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