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Selenium attenuates docetaxel-induced apoptosis and mitochondrial oxidative stress in kidney cells

Ercan Baş1, Mustafa Naziroğlu2,3

  • 1Department of Urology, Faculty of Medicine.

Anti-Cancer Drugs
|March 16, 2019
PubMed

Insights

Selenium (Se) protects kidney cells from docetaxel (DTX)-induced toxicity by reducing apoptosis and oxidative stress. This combination therapy shows promise for preventing adverse effects in normal kidney cells during cancer treatment.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Docetaxel (DTX) is a chemotherapy drug used for various cancers.
  • DTX causes adverse effects in normal tissues, particularly the kidney.
  • Selenium (Se) has shown cytoprotective effects in normal cells against DTX, but its effect on kidney cells is unexplored.

Purpose of the Study:

  • To investigate the protective effects of selenium (Se) against docetaxel (DTX)-induced nephrotoxicity.
  • To evaluate Se's impact on DTX-induced damage in normal kidney cell lines.

Main Methods:

  • Human embryonic kidney 293 (HEK293) cells were used.
  • Cells were divided into four groups: control, Se-treated, DTX-treated, and DTX+Se treated.
  • Assessed apoptosis, mitochondrial membrane potential, reactive oxygen species (ROS), lipid peroxidation, cell viability, reduced glutathione, and glutathione peroxidase.

Main Results:

  • DTX treatment increased apoptosis, mitochondrial depolarization, ROS production, and lipid peroxidation.
  • DTX decreased cell number, viability, reduced glutathione, and glutathione peroxidase.
  • Selenium treatment in the DTX+Se group reversed these DTX-induced changes, indicating protection.

Conclusions:

  • Selenium mitigates docetaxel-induced nephrotoxicity in normal kidney cells.
  • Se protects kidney cells by inhibiting apoptosis and oxidative stress, upregulating glutathione and glutathione peroxidase.
  • Combined DTX and Se therapy is a potential strategy to protect kidney cells from chemotherapy side effects.

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