ArticlePloS one2013
Addition of exogenous NAD+ prevents mefloquine-induced neuroaxonal and hair cell degeneration through reduction of caspase-3-mediated apoptosis in cochlear organotypic cultures.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 49 citations in OpenAlex.
- Epigenetic Modifications in Sensorineural Hearing Loss: Protective Mechanisms and Therapeutic Potential.Current medical science · 2025Review
- Iron Overload, Microbleeding and the Role of Bilirubin in Alzheimer's Disease Brain: Revisiting the Vascular Hypothesis.International journal of molecular sciences · 2025Review
- Sex differences in body composition, voluntary wheel running activity, balance performance, and auditory function in CBA/CaJ mice across the lifespan.Hearing research · 2023Article
- Intratympanic Administration of Dieckol Prevents Ototoxic Hearing Loss.Marine drugs · 2022Article
- Roles of Bak and Sirt3 in Paraquat-Induced Cochlear Hair Cell Damage.Neurotoxicity research · 2021Article
- The Ototoxicity of Antimalarial Drugs-A State of the Art Review.Frontiers in neurology · 2021Review
- Txn2 haplodeficiency does not affect cochlear antioxidant defenses or accelerate the progression of cochlear cell loss or hearing loss across the lifespan.Experimental gerontology · 2020Article
- New insights on repeated acoustic injury: Augmentation of cochlear susceptibility and inflammatory reaction resultant of prior acoustic injury.Hearing research · 2020Article
- Effects of Gsta4 deficiency on age-related cochlear pathology and hearing loss in mice.Experimental gerontology · 2020Article
- Some Ototoxic Drugs Destroy Cochlear Support Cells Before Damaging Sensory Hair Cells.Neurotoxicity research · 2020Article
- Antioxidative stress-induced damage in cochlear explants.Journal of otology · 2020Article
- Citicoline Protects Auditory Hair Cells Against Neomycin-Induced Damage.Frontiers in cell and developmental biology · 2020Article
- Increased burden of mitochondrial DNA deletions and point mutations in early-onset age-related hearing loss in mitochondrial mutator mice.Experimental gerontology · 2019Article
- Cochlear hair cell densities in the rabbit.Anatomical science international · 2019Article
- Differential fates of tissue macrophages in the cochlea during postnatal development.Hearing research · 2018Article
- Paraquat initially damages cochlear support cells leading to anoikis-like hair cell death.Hearing research · 2018Article
- An immortalized microglial cell line (Mocha) derived from rat cochlea.Molecular and cellular neurosciences · 2017Article
- Kanamycin Damages Early Postnatal, but Not Adult Spiral Ganglion Neurons.Neurotoxicity research · 2017Article
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Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
Abstract
backgroundMefloquine is widely used for the treatment of malaria. However, this drug is known to induce neurological side effects including depression, anxiety, balance disorder, and sensorineural hearing loss. Yet, there is currently no treatment for these side effects. PRINCIPAL
findingsIn this study, we show that the coenzyme NAD(+), known to play a critical role in maintaining the appropriate cellular redox environment, protects cochlear axons and sensory hair cells from mefloquine-induced degeneration in cultured rat cochleae. Mefloquine alone destroyed hair cells and nerve fiber axons in rat cochlear organotypics cultures in a dose-dependent manner, while treatment with NAD(+) protected axons and hair cells from mefloquine-induced degeneration. Furthermore, cochlear organs treated with mefloquine showed increased oxidative stress marker levels, including superoxide and protein carbonyl, and increased apoptosis marker levels, including TUNEL-positive nuclei and caspases-3. Treatment with NAD(+) reduced the levels of these oxidative stress and apoptosis markers. CONCLUSIONS/SIGNIFICANCE: Taken together, our findings suggest that that mefloquine disrupts the cellular redox environment and induces oxidative stress in cochlear hair cells and nerve fibers leading to caspases-3-mediated apoptosis of these structures. Exogenous NAD(+) suppresses mefloquine-induced oxidative stress and prevents the degeneration of cochlear axons and sensory hair cells caused by mefloquine treatment.
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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 Socratic graph.