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Melatonin reduces oxidative damage of neural lipids and proteins in senescence-accelerated mouse
Abstract
We investigated whether long-term melatonin administration in the drinking water influences oxidative modification of lipids and proteins and antioxidative enzyme activity in brain of senescence-accelerated mice (SAM). Cerebral cortex was obtained in the middle of the dark period of the daily light cycle from SAMP8, a strain of mice prone to accelerated senescence, and from SAMR1, a senescence-resistant strain, at 3, 6, and 12 months of age. Thiobarbituric acid-reactive substances (TBARS) and protein carbonyls exhibited significant age-related increases in both strains. Glutathione peroxidase (GPx) activity decreased significantly at 12 months of age in SAMP8. No age effect was found in GPx activity in SAMR1, or in superoxide dismutase (SOD) activity in either strain. Melatonin administration (2 microg/mL) via the drinking fluid beginning at 7 months significantly decreased neural TBARS content (over 30%) in both strains and lowered the protein carbonyl content in the brain of SAMP8 mice. Furthermore, melatonin significantly augmented GPx activity (over 20%) in both strains. Melatonin had no effect on SOD activity. These results suggest an age-related increase in cerebral tissue vulnerability to oxidation in SAM that can be modified by melatonin, most likely through the ability of melatonin to scavenge oxygen free radicals and to stimulate antioxidant enzyme activity.
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“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 [464]
In the citing paper
“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 [464]
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Self-citation
Metadata
- Authors
- Okatani, Y., Wakatsuki, A., Reiter, R. J., & Miyahara, Y.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Okatani, Yuji
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2002-07
- Volume
- 23
- Issue
- 4
- Pages
- 639-644
- ISSN
- 0197-4580 (ISSN-L)
- OpenAlex
- W2125568928
- Cited by
- 112
- References
- 45
- Citations by year
- 2023: 2 · 2022: 4 · 2021: 1 · 2019: 2 · 2018: 6 · 2016: 3 · 2015: 6 · 2014: 5 · 2013: 8 · 2012: 3
- FWCI
- 3.16
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Antioxidants, Aging, Portulaca oleracea
- Keywords
- melatonin, senescence-accelerated mice, SAMP8 mice, SAMR1, oxidative stress, lipid peroxidation, protein carbonylation, glutathione peroxidase, superoxide dismutase, antioxidant enzymes, brain aging, cerebral cortex, neuroprotection
- MeSH terms
- Aging, Animals, Female, Glutathione Peroxidase, Male, Melatonin, Oxidation-Reduction, Proteins, Superoxide Dismutase, Lipid Peroxidation, Thiobarbituric Acid Reactive Substances, Oxidative Stress, Mice
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