Nicotinamide adenine dinucleotide supplementation fails to enhance anesthetic recovery in rodents
Abstract Nicotinamide Adenine Dinucleotide (NAD+) is implicated in bioenergetics, DNA repair, and senescence. Depletion of NAD+ is associated with aging and neurodegenerative disease, prompting a growing interest in NAD+ supplementation. With rising over-the-counter use of NAD, understanding their i...
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2025-01-01
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Online Access: | https://doi.org/10.1038/s41598-024-83500-6 |
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author | Candida L. Goodnough July Montoya Erica B. Cartusciello Erin L. Floranda Eric R. Gross |
author_facet | Candida L. Goodnough July Montoya Erica B. Cartusciello Erin L. Floranda Eric R. Gross |
author_sort | Candida L. Goodnough |
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description | Abstract Nicotinamide Adenine Dinucleotide (NAD+) is implicated in bioenergetics, DNA repair, and senescence. Depletion of NAD+ is associated with aging and neurodegenerative disease, prompting a growing interest in NAD+ supplementation. With rising over-the-counter use of NAD, understanding their impact on anesthetic recovery becomes essential. This study investigates the effect of NADH, a common NAD+ precursor, on anesthesia in rodents. Baseline and post-anesthesia (1.5% isoflurane) open field and Y-maze activity were recorded in adult male and female C57BL/6 mice (n = 8–10/group). NADH (150 mg/kg, intraperitoneal) or vehicle (0.9% normal saline) were given at baseline or during anesthesia. The NADH-treated group exhibited a significant decrease in open-field activity relative to vehicle-treated. This diminished activity was reflected in reduced distance travelled and average velocity after emergence from anesthesia in the NADH-treated group. NADH treatment did not improve Y-maze performance after anesthesia, partly related to reduced locomotor activity in the NADH-treated group. This study demonstrates that NADH does not appear to hasten recovery from anesthesia. Instead, there was a depression in open-field activity and no change in Y-maze performance with NADH supplementation, indicators of locomotive and cognitive recovery in rodents. The broad implications of NAD+ in aging are likely to shape supplementation trends, highlighting the importance of understanding the potential influence of administering NAD+ on anesthetic sensitivity and recovery. |
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spelling | doaj-art-7e5fbd38ef9941c38c48f0ffe80c5caf2025-01-12T12:15:51ZengNature PortfolioScientific Reports2045-23222025-01-011511810.1038/s41598-024-83500-6Nicotinamide adenine dinucleotide supplementation fails to enhance anesthetic recovery in rodentsCandida L. Goodnough0July Montoya1Erica B. Cartusciello2Erin L. Floranda3Eric R. Gross4Department of Anesthesiology, Perioperative, and Pain Medicine, School of Medicine, Stanford UniversityDepartment of Anesthesiology, Perioperative, and Pain Medicine, School of Medicine, Stanford UniversityDepartment of Anesthesiology, Perioperative, and Pain Medicine, School of Medicine, Stanford UniversityDepartment of Anesthesiology, Perioperative, and Pain Medicine, School of Medicine, Stanford UniversityDepartment of Anesthesiology, Perioperative, and Pain Medicine, School of Medicine, Stanford UniversityAbstract Nicotinamide Adenine Dinucleotide (NAD+) is implicated in bioenergetics, DNA repair, and senescence. Depletion of NAD+ is associated with aging and neurodegenerative disease, prompting a growing interest in NAD+ supplementation. With rising over-the-counter use of NAD, understanding their impact on anesthetic recovery becomes essential. This study investigates the effect of NADH, a common NAD+ precursor, on anesthesia in rodents. Baseline and post-anesthesia (1.5% isoflurane) open field and Y-maze activity were recorded in adult male and female C57BL/6 mice (n = 8–10/group). NADH (150 mg/kg, intraperitoneal) or vehicle (0.9% normal saline) were given at baseline or during anesthesia. The NADH-treated group exhibited a significant decrease in open-field activity relative to vehicle-treated. This diminished activity was reflected in reduced distance travelled and average velocity after emergence from anesthesia in the NADH-treated group. NADH treatment did not improve Y-maze performance after anesthesia, partly related to reduced locomotor activity in the NADH-treated group. This study demonstrates that NADH does not appear to hasten recovery from anesthesia. Instead, there was a depression in open-field activity and no change in Y-maze performance with NADH supplementation, indicators of locomotive and cognitive recovery in rodents. The broad implications of NAD+ in aging are likely to shape supplementation trends, highlighting the importance of understanding the potential influence of administering NAD+ on anesthetic sensitivity and recovery.https://doi.org/10.1038/s41598-024-83500-6 |
spellingShingle | Candida L. Goodnough July Montoya Erica B. Cartusciello Erin L. Floranda Eric R. Gross Nicotinamide adenine dinucleotide supplementation fails to enhance anesthetic recovery in rodents Scientific Reports |
title | Nicotinamide adenine dinucleotide supplementation fails to enhance anesthetic recovery in rodents |
title_full | Nicotinamide adenine dinucleotide supplementation fails to enhance anesthetic recovery in rodents |
title_fullStr | Nicotinamide adenine dinucleotide supplementation fails to enhance anesthetic recovery in rodents |
title_full_unstemmed | Nicotinamide adenine dinucleotide supplementation fails to enhance anesthetic recovery in rodents |
title_short | Nicotinamide adenine dinucleotide supplementation fails to enhance anesthetic recovery in rodents |
title_sort | nicotinamide adenine dinucleotide supplementation fails to enhance anesthetic recovery in rodents |
url | https://doi.org/10.1038/s41598-024-83500-6 |
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