Evidence map›Paper›PMID 29495303›Full record

ReviewMolecules (Basel, Switzerland)2018

Mitochondria: Central Organelles for Melatonin's Antioxidant and Anti-Aging Actions.

Russel J Reiter, Dun Xian Tan, Sergio Rosales-Corral, Annia Galano, Xin Jia Zhou, Bing Xu

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
176citing papers in PubMed, 6 pooled it
17.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

176 citing papers in PubMed, 6 syntheses or guidelines pooled it, 382 citations in OpenAlex.

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  20. Melatonin: a potential target for regulating ovarian function.Archives of gynecology and obstetrics · 2025
    Review

116 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Russel J ReiterDepartment of Cellular and Structural Biology UT Health San Antonio, San Antonio, SD 78229, USA. reiter@uthscsa.edu.
Dun Xian TanDepartment of Cellular and Structural Biology UT Health San Antonio, San Antonio, SD 78229, USA. tan@uthscsa.edu.
Sergio Rosales-CorralCentro de Investigacion Biomedica de Occidente, Instituo Mexicana del Seguro Social, Guadalajara 44346, Mexico. espiral17@gmail.com.
Annia GalanoDepartamento de Quimica, Universidad Autonoma Metropolitana-Iztapatapa, Mexico D.F. 09340, Mexico. agalano@prodigy.net.mx.
Xin Jia ZhouDepartment of Cellular and Structural Biology UT Health San Antonio, San Antonio, SD 78229, USA. ZhouX4@uthscsa.edu.
Bing XuDepartment of Cellular and Structural Biology UT Health San Antonio, San Antonio, SD 78229, USA. doctxu@126.com.
The University of Texas Health Science Center at San Antonio · USMexican Social Security Institute · MXUniversidad Autónoma Metropolitana · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melatonin, along with its metabolites, have long been known to significantly reduce the oxidative stress burden of aging cells or cells exposed to toxins. Oxidative damage is a result of free radicals produced in cells, especially in mitochondria. When measured, melatonin, a potent antioxidant, was found to be in higher concentrations in mitochondria than in other organelles or subcellular locations. Recent evidence indicates that mitochondrial membranes possess transporters that aid in the rapid uptake of melatonin by these organelles against a gradient. Moreover, we predicted several years ago that, because of their origin from melatonin-producing bacteria, mitochondria likely also synthesize melatonin. Data accumulated within the last year supports this prediction. A high content of melatonin in mitochondria would be fortuitous, since these organelles produce an abundance of free radicals. Thus, melatonin is optimally positioned to scavenge the radicals and reduce the degree of oxidative damage. In light of the "free radical theory of aging", including all of its iterations, high melatonin levels in mitochondria would be expected to protect against age-related organismal decline. Also, there are many age-associated diseases that have, as a contributing factor, free radical damage. These multiple diseases may likely be deferred in their onset or progression if mitochondrial levels of melatonin can be maintained into advanced age.

Indexed as

AgingAnimalsAntioxidantsFree RadicalsHumansMelatoninMitochondriaOrgan SpecificityOxidation-ReductionOxidative PhosphorylationOxidative StressReactive Oxygen SpeciesAntioxidantsFree RadicalsMelatoninReactive Oxygen Specieselectron transport chainfree radicalsfree radical theory of agingmelatonin synthesismelatonin uptakeoxidative phosphorylationoxidative stress

Identifiers

PMID29495303
PMCPMC6017324
OpenAlexW2790776869

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.