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Doxorubicin-induced apoptosis in germinal vesicle (GV) oocytes

Hadas Bar-Joseph1, Irit Ben-Aharon, Shulamith Rizel

  • 1Department of Cell and Developmental Biology, Sackler Faculty of Medicine, Tel-Aviv University, Ramat-Aviv, Tel-Aviv, Israel.

Reproductive Toxicology (Elmsford, N.Y.)
|July 27, 2010
PubMed

Insights

Doxorubicin (DXR) chemotherapy harms ovarian germinal vesicle (GV) oocytes by crossing the blood-follicle barrier and triggering apoptosis. These GV oocytes are more vulnerable than MII oocytes, impacting fertility in cancer survivors.

Area of Science:

  • Reproductive Biology
  • Cancer Therapeutics
  • Cellular Toxicology

Background:

  • Ovarian failure is a recognized side effect of cancer treatment.
  • Doxorubicin (DXR) is a chemotherapy agent known to harm oocytes.
  • Germinal vesicle (GV) oocytes represent the majority of ovarian oocytes during chemotherapy exposure.

Purpose of the Study:

  • To characterize the effects of Doxorubicin (DXR) on germinal vesicle (GV) oocytes.
  • To investigate DXR's mechanism of toxicity in ovarian follicles.
  • To assess the vulnerability of GV oocytes compared to MII oocytes.

Main Methods:

  • In vitro exposure of mouse follicles and oocytes to DXR.
  • Fluorescence confocal microscopy for DXR localization and cellular target identification.
  • Analysis of apoptotic pathways, including mitochondrial activation, PERK, caspase-12, and PARP.

Main Results:

  • DXR penetrates the blood-follicle barrier and accumulates in oocytes and granulosa cells.
  • DXR induces apoptosis in GV oocytes via chromosomal disintegration, mitochondrial activation, ER-stress (PERK, caspase-12), and PARP inactivation.
  • Follicular GV oocytes exhibit greater sensitivity to DXR toxicity than ovulated MII oocytes.

Conclusions:

  • DXR triggers an apoptotic cascade in GV oocytes involving mitochondrial and endoplasmic reticulum (ER) stress.
  • The study elucidates DXR's mechanism of ovarian toxicity, highlighting GV oocyte vulnerability.
  • Findings suggest DXR-induced ER-stress and potential intracellular calcium increase contribute to oocyte apoptosis.

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