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Updated: Jun 2, 2026
Human Primary Trophoblast Cell Culture Model to Study the Protective Effects of Melatonin Against Hypoxia/reoxygenation-induced Disruption
Published on: July 30, 2016
Melatonin protects human spermatozoa from apoptosis via melatonin receptor- and extracellular signal-regulated
Javier Espino1, Águeda Ortiz, Ignacio Bejarano
1Department of Physiology, Neuroimmunophysiology and Chrononutrition Research Group, Faculty of Science, University of Extremadura, Badajoz, Spain.
Objective:
To evaluate whether the protective effect of melatonin on H2O2-induced caspase activation and DNA fragmentation depends on the interaction between melatonin and its surface receptors.
Design:
Laboratory study.
Setting:
Center for assisted human reproduction at a Spanish hospital.
Patient(S):
Twenty-one healthy donors.
Intervention(S):
Human spermatozoa were treated with increasing concentrations of hydrogen peroxide (H2O2; 1 μM, 10 μM, 100 μM, 1 mM) and preincubated with 1 mM melatonin.
Main Outcomes Measure(S):
Activation of caspase-3 and -9 as well as DNA fragmentation were examined by fluorescence methods.
Result(S):
Our findings showed that H2O2 induced a significant increase in caspase-9 and caspase-3, which was dose independent. Conversely, pretreatment with melatonin reduced H2O2-mediated caspase activation in a dose-dependent way. Moreover, the antiapoptotic effects of melatonin in ejaculated human spermatozoa may involve membrane melatonin receptor MT1. In addition, we found that the survival-promoting pathway extracellular signal-regulated kinase (ERK) is likely to have a role in the protective actions of melatonin in ejaculated human spermatozoa. Finally, we confirmed these results further by demonstrating that melatonin prevention of H2O2-induced DNA fragmentation is dependent on both MT1 receptor and ERK signaling.
Conclusion(S):
These results indicate that the stimulation with melatonin triggers a set of events culminating in cell death prevention in ejaculated human spermatozoa.
Insights
Melatonin protects human sperm from oxidative stress by activating the MT1 receptor and ERK pathway, preventing caspase activation and DNA damage. This research highlights melatonin
Area of Science:
- Reproductive biology
- Oxidative stress research
- Cell signaling
Background:
- Oxidative stress negatively impacts sperm function and DNA integrity.
- Melatonin is a known antioxidant with potential protective effects on cells.
Purpose of the Study:
- To investigate if melatonin's protective effects against hydrogen peroxide (H2O2)-induced damage in human sperm are mediated by its surface receptors.
- To elucidate the role of melatonin receptor MT1 and the extracellular signal-regulated kinase (ERK) pathway in melatonin's protective mechanism.
Main Methods:
- Human spermatozoa were exposed to varying concentrations of H2O2.
- Spermatozoa were pretreated with melatonin.
- Caspase activation and DNA fragmentation were measured using fluorescence assays.
Main Results:
- Hydrogen peroxide (H2O2) significantly increased caspase-9 and caspase-3 activation in a dose-independent manner.
- Melatonin pretreatment dose-dependently reduced H2O2-induced caspase activation.
- Melatonin's antiapoptotic effects and prevention of DNA fragmentation were dependent on the MT1 receptor and ERK signaling.
Conclusions:
- Melatonin prevents H2O2-induced apoptosis and DNA fragmentation in human spermatozoa.
- The protective mechanism involves the MT1 receptor and the ERK signaling pathway.
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