title: Lactoferrin is associated with a decrease in oocyte depletion in mice receiving cyclophosphamide.
abstract: OBJECTIVE
  To investigate new important molecules involved in the regulation of chemotherapy-induced ovarian damage and, based on those results, to examine the effect of lactoferrin on cyclophosphamide (CPM)-induced ovarian failure.
  
  
  METHODS
  Complementary DNA microarray and the administration of lactoferrin.
  
  
  METHODS
  Experimental animal study.
  
  
  METHODS
  Female imprinting control region mice.
  
  
  METHODS
  Administration of CPM to mice, isolation of ovaries, isolation of RNA, microarray hybridization, and statistical analysis. According to the results of the microarray assay, administration of lactoferrin to CPM-treated mice, isolation of ovaries, isolation of RNA, and evaluation using quantitative polymerase chain reaction and histomorphometric analyses.
  
  
  METHODS
  A list of nine down-regulated and two up-regulated genes with reliable hybridization signals was obtained. Several target molecules were then investigated.
  
  
  RESULTS
  Among the listed genes, we focused on the mouse lactoferrin gene, because of its CPM-induced expression pattern and its multiple novel functions. Oral administration of bovine lactoferrin prevented down-regulation of the ovulation-related, Adamts1 and partial recovery of follicle depletion induced by CPM treatment.
  
  
  CONCLUSIONS
  The present report suggests that lactoferrin helps to rescue the ability to ovulate and partially to prevent oocyte depletion in mouse ovaries.
authors.affiliation: Department of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
authors.forename: Yuka
authors.initials: Y
authors.lastname: Horiuchi
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Higuchi
authors.forename: Keiji
authors.initials: K
authors.lastname: Tatsumi
authors.forename: Kenji
authors.initials: K
authors.lastname: Takakura
authors.forename: Shingo
authors.initials: S
authors.lastname: Fujii
authors.forename: Ikuo
authors.initials: I
authors.lastname: Konishi
mesh_terms: D000818:Animals; D015925:Cryopreservation / Q000379:methods; D003520:Cyclophosphamide / Q000494:pharmacology*; D018076:DNA, Complementary / Q000235:genetics; D004622:Embryo, Mammalian / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D005260:Female; D000071316:Forkhead Box Protein O3; D051858:Forkhead Transcription Factors / Q000235:genetics; D006064:Gonadotropins, Equine / Q000633:toxicity; D007781:Lactoferrin / Q000235:genetics* / Q000502:physiology; D051379:Mice; D008813:Mice, Inbred ICR; D020411:Oligonucleotide Array Sequence Analysis; D009865:Oocytes / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D010053:Ovary / Q000473:pathology / Q000502:physiology; D010060:Ovulation / Q000502:physiology; D011247:Pregnancy; D016649:Primary Ovarian Insufficiency / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D012333:RNA, Messenger / Q000235:genetics
chemical_list: D018076:DNA, Complementary; D000071316:Forkhead Box Protein O3; D051858:Forkhead Transcription Factors; C474033:FoxO3 protein, mouse; D006064:Gonadotropins, Equine; D012333:RNA, Messenger; D003520:Cyclophosphamide; D007781:Lactoferrin