Intraovarian transplantation of primordial follicles fails to rescue chemotherapy injured ovaries

Sci Rep. 2013:3:1384. doi: 10.1038/srep01384.

Abstract

Busulfan and cyclophosphamide (B/C)-treated mice exhibited a marked increase in apoptosis and a concomitant decrease in the ovarian weight. Histological and RT-PCR analysis indicate that the period of germ cell depletion in the B/C-treated ovaries coincides with decreased expression of genes Figla, Lhx8, Nobox, c-kit, and Sox3. However, depletion of the ovarian germ cells is mediated by autophagy-independent pathways that involve Fas/FasL-, TNF-, and/or p53-signalings. Treatment with B/C resulted in the cease of the reproductive function to produce their offspring during the 15(th) week post-treatment period in female mice. Furthermore, injection of the 3 × 10(6) GFP positive primordial follicles into the ovaries of the B/C treated mouse did not show apparent colonization of the transplanted follicles within the recipient ovaries. The present results suggest that B/C treatment is closely associated with an increased risk of premature ovarian failure.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Agents / administration & dosage
  • Antineoplastic Agents / adverse effects*
  • Apoptosis / drug effects
  • Apoptosis / genetics
  • Biomarkers
  • Busulfan / administration & dosage
  • Busulfan / adverse effects
  • Cyclophosphamide / administration & dosage
  • Cyclophosphamide / adverse effects
  • Fas Ligand Protein / genetics
  • Fas Ligand Protein / metabolism
  • Female
  • Gene Expression Regulation
  • Male
  • Mice
  • Oocytes / drug effects
  • Oocytes / metabolism
  • Ovarian Follicle / metabolism
  • Ovarian Follicle / transplantation*
  • Ovary / drug effects*
  • Ovary / pathology
  • Ovary / surgery*
  • Ovum / drug effects
  • Proto-Oncogene Proteins c-kit / genetics
  • Proto-Oncogene Proteins c-kit / metabolism
  • Reproduction / drug effects
  • Signal Transduction
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • fas Receptor / genetics
  • fas Receptor / metabolism

Substances

  • Antineoplastic Agents
  • Biomarkers
  • Fas Ligand Protein
  • Tumor Necrosis Factor-alpha
  • Tumor Suppressor Protein p53
  • fas Receptor
  • Cyclophosphamide
  • Proto-Oncogene Proteins c-kit
  • Busulfan