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Published on: December 28, 2021
Hesperidin attenuates gentamicin-induced testicular toxicity via modulation of the PI3K/AKT signaling pathway
Murat Celebi1, Cagla Celebi2, Hasan Susar3
1Department of Veterinary, Savaştepe Vocational School, Balıkesir University, Balıkesir, Türkiye. murat.celebi@balikesir.edu.tr.
Background:
Gentamicin is an aminoglycoside antibiotic widely used in the treatment of Gram-negative infections; however, one of its major limitations is testicular toxicity. Oxidative stress is considered to play a central role in gentamicin-induced testicular damage. Hesperidin is a natural flavonoid with potent antioxidant and cytoprotective properties and may exert protective effects on the reproductive system.
Methods:
This study investigated the protective effects of hesperidin against gentamicin-induced testicular damage. Histopathological and immunohistochemical evaluations were performed alongside biochemical and hormonal analyses. In addition, sperm concentration, motility, and the rate of abnormal spermatozoa were assessed. To elucidate the underlying molecular mechanisms, the gene expression levels of PD-1, PI3K, and AKT-1 were analyzed.
Results:
Gentamicin administration was associated with lower Johnsen scores, decreased testosterone levels and sperm motility, increased sperm abnormalities, elevated MDA concentrations, reduced CAT, SOD, GPx, and GSH levels, increased Caspase-3 and 8-OHdG immunoreactivity, and reduced AKT expression. Hesperidin co-administration significantly attenuated many of these alterations, being associated with improved histopathological scores, enhanced antioxidant status, reduced immunoreactivity of oxidative stress- and apoptosis-related markers, improved sperm quality parameters, and increased PI3K and AKT gene expression compared with the gentamicin-treated group.
Conclusion:
These findings indicate that hesperidin possesses a protective potential against gentamicin-induced testicular damage, likely mediated through its antioxidant and anti-apoptotic effects.
Insights
Hesperidin, a natural antioxidant, protects against gentamicin-induced testicular toxicity by reducing oxidative stress and apoptosis. This study shows hesperidin improves sperm quality and reproductive health markers.
Area of Science:
- Reproductive toxicology
- Pharmacology
- Natural product chemistry
Background:
- Gentamicin, an antibiotic for Gram-negative infections, causes testicular toxicity.
- Oxidative stress is a key factor in gentamicin-induced testicular damage.
- Hesperidin, a flavonoid, exhibits antioxidant and cytoprotective properties.
Purpose of the Study:
- To evaluate the protective effects of hesperidin against gentamicin-induced testicular damage.
- To investigate the molecular mechanisms underlying hesperidin's protective action.
Main Methods:
- Histopathological and immunohistochemical analyses were conducted.
- Biochemical assays measured oxidative stress markers (MDA, CAT, SOD, GPx, GSH).
- Hormonal levels, sperm parameters (concentration, motility, abnormalities), and gene expression (PD-1, PI3K, AKT-1) were assessed.
Main Results:
- Gentamicin induced testicular damage, reduced sperm quality, and altered antioxidant/apoptotic markers.
- Hesperidin co-administration improved histopathology, antioxidant status, and sperm parameters.
- Hesperidin increased PI3K and AKT gene expression while reducing oxidative stress and apoptosis markers.
Conclusions:
- Hesperidin demonstrates significant protective potential against gentamicin-induced testicular toxicity.
- The protective effects are likely mediated by hesperidin's antioxidant and anti-apoptotic properties.
- Hesperidin may represent a therapeutic strategy to mitigate gentamicin's reproductive side effects.
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