Studies on the ameliorative potential of dietary supplemented selenium on doxorubicin-induced testicular damage in

Sarvnarinder Kaur1, Khushpreet Singh Maan1, Shilpa Sadwal1

  • 1Department of Biophysics, Panjab University, Chandigarh, India.

Andrologia
|October 28, 2020
PubMed

Insights

Dietary selenium supplementation can protect against doxorubicin-induced testicular damage in mice. Selenium reduces oxidative stress and apoptosis, improving sperm parameters and testicular health.

Area of Science:

  • Reproductive Toxicology
  • Oxidative Stress Research
  • Nutritional Biochemistry

Background:

  • Doxorubicin (chemotherapeutic agent) induces testicular damage via oxidative stress, impairing spermatogenesis.
  • Oxidative stress disrupts sperm parameters, testicular histology, and germ cell kinetics.

Purpose of the Study:

  • To investigate the protective effects of dietary selenium against doxorubicin-induced testicular toxicity in mice.
  • To evaluate selenium's impact on oxidative stress markers, antioxidant levels, and apoptotic pathways in the testes.

Main Methods:

  • Mice were divided into four groups: control, selenium-supplemented, doxorubicin-treated, and selenium + doxorubicin-treated.
  • Evaluated sperm parameters, testicular histopathology, germ cell kinetics, oxidative stress, and antioxidant levels.
  • Analyzed mRNA expression of apoptotic and stress response markers.

Main Results:

  • Doxorubicin treatment significantly reduced sperm parameters and increased oxidative stress markers.
  • Selenium supplementation ameliorated doxorubicin-induced testicular damage, improving sperm quality and histology.
  • Selenium reduced oxidative stress, increased antioxidant levels, and decreased apoptotic markers in doxorubicin-treated mice.

Conclusions:

  • Dietary selenium exhibits a curative effect against doxorubicin-induced testicular damage.
  • Selenium mitigates testicular toxicity by attenuating oxidative stress and apoptosis.
  • Selenium supplementation is a potential therapeutic strategy for doxorubicin-induced reproductive toxicity.

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