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Cited by 112Circadian rhythm and melatoninAntioxidant Activity and Oxidative StressAntioxidants, Aging, Portulaca oleracea

The DOI matches its Crossref record; 41 of the 45 references it cites were found in a registry or an index.

Melatonin reduces oxidative damage of neural lipids and proteins in senescence-accelerated mouse

Okatani, Yuji, Wakatsuki, Akihiko, Reiter, Russel J., Miyahara, Yasuyo·2002·Neurobiology of Aging
DOI 10.1016/s0197-4580(02)00005-2
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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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Research works printed but not linked: 3

  1. Pablos, 1997, Both melatonin and a putative nuclear melatonin receptor agonist CGP 52608 stimulate glutathione peroxidase, and glutathione reductase activities in mouse brain in vivo, Neuroendocrinol Lett, 18, 49
  2. Reiter, 1992, The aging pineal gland and itsphysiological consequences, Bio Essays, 14, 169
  3. Tan, 1993, Melatonin, Endocr J, 1, 57

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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
ORCID
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2002-07
Volume
23
Issue
4
Pages
639-644
ISSN
0197-4580 (ISSN-L)
DOI
10.1016/s0197-4580(02)00005-2
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
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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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