Cited by 100Circadian rhythm and melatoninMitochondrial Function and PathologyParkinson's Disease Mechanisms and Treatments

Melatonin in mitochondrial dysfunction and related disorders

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Srinivasan, Venkatramanujam, Spence, D. Warren, Pandi-Perumal, Seithikurippu R., Brown, Gregory M., Cardinali, Daniel P.·2011·International Journal of Alzheimer s Disease

Abstract

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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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
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
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

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