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Updated: Jan 2, 2026
Imaging Approaches to Assessments of Toxicological Oxidative Stress Using Genetically-encoded Fluorogenic Sensors
Published on: February 7, 2018
Fluoride Compromises Testicular Redox Sensor, Gap Junction Protein, and Metabolic Status: Amelioration by Melatonin
Jitendra Kumar1, Chandana Haldar1, Rakesh Verma2
1Department of Zoology, Pineal Research Laboratory, Reproduction Biology Unit, Institute of Science, Banaras Hindu University, Varanasi, U.P., 221005, India.
Abstract:
The excess fluoride intake has been shown to adversely affect male reproductive health. The aim of the present study was to investigate the key mechanism underlying fluoride-induced testicular dysfunction and the role of melatonin as a modulator of testicular metabolic, oxidative, and inflammatory load. The present results indicated that sodium fluoride (NaF) exposure to adult male golden hamsters severely impairs reproductive physiology as evident from markedly reduced sperm count/viability, testosterone level, androgen receptor (AR), testicular glucose transporter (GLUT-1), gap junction (connexin-43), and survival (Bcl-2) protein expression. NaF exposure markedly increased testicular oxidative load, inflammatory (NF-kB/COX-2), and apoptotic (caspase-3) protein expression. However, melatonin treatment remarkably restored testicular function as evident by normal histoarchitecture, increased sperm count/viability, enhanced antioxidant enzyme activities (SOD and Catalase), and decreased lipid peroxidation (LPO) level. In addition, melatonin treatment upregulated testicular Nrf-2/HO-I, SIRT-1/ FOXO-1, and downregulated NF-kB/COX-2 expression. Further, melatonin ameliorated NaF-induced testicular metabolic stress by modulating testicular GLUT-1expression, glucose level, and LDH activity. Furthermore, melatonin treatment enhanced testicular PCNA, Bcl-2, connexin-43, and reduced caspase-3 expression. In conclusion, we propose the molecular mechanism of fluoride-induced testicular damages and ameliorative action(s) of melatonin.
Insights
Excess fluoride intake harms male reproductive health. Melatonin treatment protected against fluoride-induced testicular damage by reducing oxidative stress and inflammation.
Area of Science:
- Reproductive Toxicology
- Endocrinology
- Biochemistry
Background:
- Excessive fluoride intake is linked to adverse effects on male reproductive health.
- Understanding the mechanisms of fluoride-induced testicular dysfunction is crucial.
Purpose of the Study:
- To investigate the molecular mechanisms of fluoride-induced testicular dysfunction.
- To evaluate the protective role of melatonin against fluoride toxicity in male hamsters.
Main Methods:
- Adult male golden hamsters were exposed to sodium fluoride (NaF).
- Melatonin treatment was administered to assess its modulatory effects.
- Key reproductive, oxidative stress, inflammatory, and apoptotic markers were analyzed.
Main Results:
- NaF exposure significantly reduced sperm count/viability, testosterone levels, and expression of AR, GLUT-1, connexin-43, and Bcl-2.
- NaF increased oxidative stress, inflammation (NF-kB/COX-2), and apoptosis (caspase-3).
- Melatonin treatment restored testicular function, improved antioxidant status, and modulated key molecular pathways.
Conclusions:
- Fluoride induces testicular damage through metabolic, oxidative, and inflammatory pathways.
- Melatonin effectively ameliorates fluoride-induced testicular toxicity by targeting these pathways.
- This study elucidates the molecular mechanisms of fluoride's reproductive toxicity and melatonin's protective effects.
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