Effect of melatonin supplementation on oxidative stress parameters: A systematic review and meta-analysis
Effect of melatonin supplementation on oxidative stress parameters: A systematic review and meta-analysis
Morvaridzadeh et al., 2020 | Pharmacol Res | Meta Analysis
Citation
Morvaridzadeh Mojgan, Sadeghi Ehsan, ... Heshmati Javad. Effect of melatonin supplementation on oxidative stress parameters: A systematic review and meta-analysis. Pharmacol Res. 2020-Nov;161:105210. doi:10.1016/j.phrs.2020.105210
Abstract
BACKGROUND: Oxidative stress, defined as an imbalance between pro-oxidants and neutralizing antioxidants within the body, is a growing public health concern. Oxidative stress is involved in the progression of nearly all chronic diseases. Melatonin has been suggested to reduce oxidative stress by its potential radical scavenging properties. OBJECTIVE: To determine the efficacy and safety of melatonin as a therapy for the improvement of oxidative stress parameters in randomized controlled trials. METHODS: A systematic database search using Scopus, PubMed/Medline, EMBASE, Web of Science, the Cochrane Controlled Register of Trials and clinicaltrials.gov (https://clinicaltrials.gov) for studies published up to July 2020 was conducted. We included studies which investigated the effect of supplemental melatonin compared to placebo on oxidative stress parameters in unhealthy patients. Quantitative data synthesis was conducted using a random-effects model with standard mean difference (SMD) and 95 % confidence intervals (CI). Cochrane's Q and I2 values were used to evaluate heterogeneity. RESULTS: A total of 12 randomized controlled trials (RCTs) were eligible. The meta-analysis indicated an association between melatonin intake and a significant increase in total antioxidant capacity (TAC) (SMD: 0.76; 95 % CI: 0.30, 1.21; I2 = 80.1 %), glutathione (GSH) levels (SMD: 0.57; 95 % CI: 0.32, 0.83; I2 = 15.1 %), superoxide dismutase (SOD) (SMD: 1.38; 95 % CI: 0.13, 2.62; I2 = 86.9 %), glutathione peroxidase (GPx) (SMD: 1.36; 95 % CI: 0.46, 2.30; I2 = 89.3 %), glutathione reductase (GR) (SMD: 1.21; 95 % CI: 0.65, 1.77; I2 = 00.0 %) activities, and a significant reduction in malondialdehyde (MDA) levels (SMD: -0.79; 95 % CI: -1.19, -0.39; I2 = 73.1 %). Melatonin intake was not shown to significantly affect nitric oxide (NO) levels (SMD: -0.24; 95 % CI: -0.61, 0.14; I2 = 00.0 %) or catalase (CAT) activity (SMD: -1.38; 95 % CI: -1.42, 4.18; I2 = 96.6 %). CONCLUSION: Melatonin intake was shown to have a significant impact on improving Oxidative stress parameters. However, future research through large, well-designed randomized controlled trials are required to determine the effect of melatonin on oxidative stress parameters in different age groups and different disease types.
Key Findings
A total of 12 randomized controlled trials (RCTs) were eligible. The meta-analysis indicated an association between melatonin intake and a significant increase in total antioxidant capacity (TAC) (SMD: 0.76; 95 % CI: 0.30, 1.21; I2 = 80.1 %), glutathione (GSH) levels (SMD: 0.57; 95 % CI: 0.32, 0.83; I2 = 15.1 %), superoxide dismutase (SOD) (SMD: 1.38; 95 % CI: 0.13, 2.62; I2 = 86.9 %), glutathione peroxidase (GPx) (SMD: 1.36; 95 % CI: 0.46, 2.30; I2 = 89.3 %), glutathione reductase (GR) (SMD: 1.
Outcomes Measured
- Requires manual extraction
Population
| Field | Value |
|---|---|
| Population | See abstract |
| Sample Size | See abstract |
| Age Range | See abstract |
| Condition | stress |
MeSH Terms
- Adolescent
- Adult
- Aged
- Antioxidants
- Biomarkers
- Catalase
- Child
- Dietary Supplements
- Female
- Glutathione
- Glutathione Peroxidase
- Glutathione Reductase
- Humans
- Lipid Peroxidation
- Male
- Malondialdehyde
- Melatonin
- Middle Aged
- Nitric Oxide
- Oxidative Stress
- Randomized Controlled Trials as Topic
- Superoxide Dismutase
- Treatment Outcome
- Young Adult
Evidence Classification
- Level: Meta Analysis
- Publication Types: Journal Article, Meta-Analysis, Systematic Review
- Vertical: melatonin
Provenance
- PMID: 33007423
- DOI: 10.1016/j.phrs.2020.105210
- PMCID: Not in PMC
- Verified: 2026-04-09 via PubMed E-utilities API
Source extracted via PubMed E-utilities API on 2026-04-09