Melatonin in mitochondrial dysfunction and related disorders
Open accessAbstract
Mitochondrial dysfunction is considered one of the major causative factors in the aging process, ischemia/reperfusion (I/R), septic shock, and neurodegenerative disorders like Parkinson's disease (PD), Alzheimer's disease (AD), and Huntington's disease (HD). Increased free radical generation, enhanced mitochondrial inducible nitric oxide (NO) synthase activity, enhanced NO production, decreased respiratory complex activity, impaired electron transport system, and opening of mitochondrial permeability transition pore all have been suggested as factors responsible for impaired mitochondrial function. Melatonin, the major hormone of the pineal gland, also acts as an antioxidant and as a regulator of mitochondrial bioenergetic function. Both in vitro and in vivo, melatonin was effective for preventing oxidative stress/nitrosative stress-induced mitochondrial dysfunction seen in experimental models of PD, AD, and HD. In addition, melatonin is known to retard aging and to inhibit the lethal effects of septic shock or I/R lesions by maintaining respiratory complex activities, electron transport chain, and ATP production in mitochondria. Melatonin is selectively taken up by mitochondrial membranes, a function not shared by other antioxidants. Melatonin has thus emerged as a major potential therapeutic tool for treating neurodegenerative disorders such as PD or AD, and for preventing the lethal effects of septic shock or I/R.
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Mitochondrial membranes selectively take up melatonin, a function not shared by other antioxidants.
“Mitochondrial membranes selectively take up melatonin, a function not shared by other antioxidants [63].”
From Is Melatonin the “Next Vitamin D”?: A Review of Emerging Science, Clinical Uses, Safety, and Dietary Supplements (2022) · cites this paper as [63]
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Mander, P. K., & Brown, G. C. (2004) · Biochemical Society Transactions · doi:10.1042/bst0321068 · Cited by 35 · see citing works
Self-citationBobba, A., Petragallo, V. A., Marra, E., & Atlante, A. (2010) · International Journal of Alzheimer s Disease · doi:10.4061/2010/621870 · Cited by 34 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Minich, D. M., Henning, M., Darley, C., Fahoum, M., Schuler, C. B., & Frame, J. (2022) · Nutrients · doi:10.3390/nu14193934 · Cited by 176 · see citing works
“Mitochondrial membranes selectively take up melatonin, a function not shared by other antioxidants [63].”
BackgroundA model of the mitochondrial basis of bipolar disorder
Morris, G., Walder, K., McGee, S. L., Dean, O. M., Tye, S. J., Maes, M., & Berk, M. (2017) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2017.01.014 · Cited by 162 · see citing works
Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration
Jha, S. K., Jha, N. K., Kumar, D., Ambasta, R. K., & Kumar, P. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.06.015 · Cited by 122 · see citing works
- Authors
- Srinivasan, V., Spence, D. W., Pandi-Perumal, S. R., Brown, G. M., & Cardinali, D. P.
- Affiliations
- Centre for Addiction and Mental Health (CA)
- Universidad de Buenos Aires (AR)
- Corresponding author
- Cardinali, Daniel P.
- Venue
- International Journal of Alzheimer s Disease
- Publisher
- Wiley
- Published
- 2011-01
- Volume
- 2011
- Issue
- 1
- Pages
- 326320-326320
- ISSN
- 2090-0252 (ISSN-L)
- 2090-8024
- PMC
- PMC3100547
- OpenAlex
- W2039960515
- Cited by
- 100
- References
- 210
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 8 · 2023: 6 · 2022: 2 · 2021: 7 · 2020: 6 · 2019: 9 · 2018: 6 · 2017: 8 · 2016: 6 · 2015: 6 · 2014: 12 · 2013: 8 · 2012: 7
- FWCI
- 4.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- International Journal of Alzheimer s Disease (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- Americanae (AECID Library) (submittedVersion, cc-by-nc-sa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- CONICET Digital (CONICET) (submittedVersion, cc-by-nc-sa)
- Greater South Information System
- Funders
- Consejo Nacional de Investigaciones Científicas y Técnicas
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- melatonin, mitochondrial dysfunction, neurodegenerative diseases, Parkinson's disease, Alzheimer's disease, Huntington's disease, aging, ischemia-reperfusion injury, septic shock, oxidative stress, nitrosative stress, mitochondrial permeability transition pore, electron transport chain, nitric oxide synthase, antioxidants, mitochondrial bioenergetics
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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