Chronic Melatonin Administration Reduced Oxidative Damage and Cellular Senescence in the Hippocampus of a Mouse Model of Down Syndrome
Open accessAbstract
Previous studies have demonstrated that melatonin administration improves spatial learning and memory and hippocampal long-term potentiation in the adult Ts65Dn (TS) mouse, a model of Down syndrome (DS). This functional benefit of melatonin was accompanied by protection from cholinergic neurodegeneration and the attenuation of several hippocampal neuromorphological alterations in TS mice. Because oxidative stress contributes to the progression of cognitive deficits and neurodegeneration in DS, this study evaluates the antioxidant effects of melatonin in the brains of TS mice. Melatonin was administered to TS and control mice from 6 to 12 months of age and its effects on the oxidative state and levels of cellular senescence were evaluated. Melatonin treatment induced antioxidant and antiaging effects in the hippocampus of adult TS mice. Although melatonin administration did not regulate the activities of the main antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione S-transferase) in the cortex or hippocampus, melatonin decreased protein and lipid oxidative damage by reducing the thiobarbituric acid reactive substances (TBARS) and protein carbonyls (PC) levels in the TS hippocampus due to its ability to act as a free radical scavenger. Consistent with this reduction in oxidative stress, melatonin also decreased hippocampal senescence in TS animals by normalizing the density of senescence-associated β-galactosidase positive cells in the hippocampus. These results showed that this treatment attenuated the oxidative damage and cellular senescence in the brain of TS mice and support the use of melatonin as a potential therapeutic agent for age-related cognitive deficits and neurodegeneration in adults with DS.
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Evidence is contrasting about the effect of melatonin on regulation of antioxidant enzymes.
“However, contrasting evidence remains about the effect of melatonin on the regulation of antioxidant enzymes [457,463,464,465].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [463]
In vivo, melatonin intake diminishes age-derived inflammation and apoptosis, decreases lipid peroxidation, TBARS, and protein carbonyls, counteracting hippocampal senescence and exerting anti-aging and antioxidant effects on mice brains.
“In vivo, melatonin intake has been reported to diminish age-derived inflammation and apoptosis and to decrease lipid peroxidation, thiobarbituric acid reactive substances and protein carbonyls, thus counteracting hippocampal senescence and exerting an anti-aging and antioxidant effect on mice brains [462,463,464,465].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [463]
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References 51 · Cited by 37
- Authors
- Parisotto, E. B., Vidal, V., García-Cerro, S., Lantigua, S., Wilhelm Filho, D., Sanchez-Barceló, E. J., Martínez-Cué, C., & Rueda, N.
- Affiliations
- Universidade Federal de Santa Catarina (BR)
- Universidad de Cantabria (ES)
- Venue
- Neurochemical Research
- Published
- 2016-07-23
- Volume
- 41
- Issue
- 11
- Pages
- 2904-2913
- ISSN
- 0364-3190 (ISSN-L)
- 1573-6903
- OpenAlex
- W2481568171
- Cited by
- 37
- References
- 51
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 9 · 2022: 3 · 2021: 5 · 2020: 4 · 2019: 3 · 2018: 3 · 2017: 4
- FWCI
- 2.12
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- Locations
- Neurochemical Research (publishedVersion)
- PubMed (publishedVersion)
- UCrea (University of Cantabria) (acceptedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Antioxidants, Aging, Portulaca oleracea
- Keywords
- melatonin, Down syndrome, Ts65Dn mouse model, hippocampus, oxidative stress, cellular senescence, senescence-associated β-galactosidase, lipid peroxidation, protein carbonylation, antioxidant enzymes, neurodegeneration, age-related cognitive decline, anti-aging
- MeSH terms
- Animals, Antioxidants, Disease Models, Animal, Down Syndrome, Glutathione Peroxidase, Glutathione Reductase, Glutathione Transferase, Hippocampus, Melatonin, Oxidation-Reduction, Superoxide Dismutase, Cellular Senescence, Thiobarbituric Acid Reactive Substances, Long-Term Potentiation, Oxidative Stress, Mice
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