title: Developmental blockage of mouse embryos caused by fatty acids.
abstract: OBJECTIVE
  It has been shown that lipid peroxides derived from polyunsaturated fatty acids (PUFAs) inhibit the proliferation of various cells. In the meantime, it has been suggested that oxidative stress is closely related to the developmental blockage of mammalian embryos cultured in vitro. In this study, we investigated the effects by various fatty acids on mouse embryo development in vitro, and the reversal of these effects by various antioxidants such as superoxide dismutase, ascorbic acid, alpha-tocopherol, uric acid, and ethylenediaminetetraacetic acid.
  
  
  METHODS
  Pronuclear and two-cell stage mouse (ICR) embryos were cultured in Biggers-Whitten-Whittingham medium with 0.3% bovine serum albumin alone or complexed with one of the following fatty acids: palmitic, stearic, oleic, linoleic, linolenic, or arachidonic acid. We also measured the fluorescence emission of embryos in media containing various fatty acids in order to investigate the involvement of H2O2 or lipid peroxidation in embryo development.
  
  
  RESULTS
  Palmitic acid and PUFAs including linoleic acid inhibited the embryo development. The inhibitory effect of PUFAs was attenuated by adding antioxidants into the media, while the inhibitory effect of palmitic acid was not. Both pronuclear and two-cell stage embryos with PUFAs showed markedly more intensive emissions than those under other conditions.
  
  
  CONCLUSIONS
  These results suggest that lipid radicals can easily be generated in early stage embryos and that blastomeres are among the cells vulnerable to the damage by lipid peroxidation.
authors.affiliation: Department of Gynecology and Obstetrics, Kyoto University, Faculty of Medicine, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Nonogaki
authors.forename: Y
authors.initials: Y
authors.lastname: Noda
authors.forename: Y
authors.initials: Y
authors.lastname: Goto
authors.forename: J
authors.initials: J
authors.lastname: Kishi
authors.forename: T
authors.initials: T
authors.lastname: Mori
mesh_terms: D000818:Animals; D016718:Arachidonic Acid / Q000494:pharmacology; D001205:Ascorbic Acid / Q000494:pharmacology; D002455:Cell Division / Q000502:physiology; D004492:Edetic Acid / Q000494:pharmacology; D005314:Embryonic and Fetal Development / Q000187:drug effects* / Q000502:physiology; D005227:Fatty Acids / Q000494:pharmacology*; D005260:Female; D005453:Fluorescence; D006859:Hydrogen / Q000502:physiology; D019787:Linoleic Acid; D008041:Linoleic Acids / Q000494:pharmacology; D015227:Lipid Peroxidation; D051379:Mice; D008813:Mice, Inbred ICR; D019301:Oleic Acid; D009829:Oleic Acids / Q000494:pharmacology; D019308:Palmitic Acid; D010169:Palmitic Acids / Q000494:pharmacology; D013229:Stearic Acids / Q000494:pharmacology; D013482:Superoxide Dismutase / Q000494:pharmacology; D014527:Uric Acid / Q000494:pharmacology; D014810:Vitamin E / Q000494:pharmacology; D017962:alpha-Linolenic Acid / Q000494:pharmacology
chemical_list: D005227:Fatty Acids; D008041:Linoleic Acids; D009829:Oleic Acids; D010169:Palmitic Acids; D013229:Stearic Acids; D017962:alpha-Linolenic Acid; D014810:Vitamin E; D014527:Uric Acid; D016718:Arachidonic Acid; D019301:Oleic Acid; D019308:Palmitic Acid; C031183:stearic acid; D006859:Hydrogen; D004492:Edetic Acid; D019787:Linoleic Acid; D013482:Superoxide Dismutase; D001205:Ascorbic Acid