title: Comparison of lens biochemistry and structure between BSO-treated and glucocorticoid-treated developing chick embryos.
abstract: In this paper various changes in glutathione level, which were influenced by balance of its synthesis, degradation, transport and utilization, were analysed in chick embryos administered with glucocorticoid (GC) or buthionine sulfoximine (BSO; an inhibitor of glutathione synthesis). When BSO (30 mumol egg-1) was administered twice to chick embryos on day 14 and 15, the GSH in both the lens and the liver decreased to 15-20% and 30-40% of the age-matched control level, respectively, between 24 and 48 hr after the second treatment, then began to recover. Although this decline in the GSH level in these tissues was greater and more prolonged in embryos treated with BSO than with GC, the former embryos maintained lens transparency even up to 144 hr by a visual examination. However, histological changes in the lens occurred after 96 hr and more significantly 144 hr after second administration of BSO. The changes mainly consisted of pale epithelial cells on the anterior peripheral surface of the lens, irregular height of the epithelial cells at the equator, clefts between the epithelium and the cortex and swelling of almost all the cortical fibers. These observations may suggest that BSO treatment could produce the beginning of a cataract. Embryos with GC-cataract revealed the following changes at 48 hr: loss of transparency, elevation of LPO (TBA-reacting substance) in the lens, the blood and the liver. These were not observed in BSO-treated embryos during the experimental period. The GC-cataract may well depend on the generation of LPO. BSO cataract, having a distinct mechanism compared to that caused by GC, develops more slowly in GSH-depleted lenses. The BSO-treated chick embryos will be a useful model to screen the risk factors which accelerate cataract formation.
authors.affiliation: Faculty of Pharmaceutical Sciences, Teikyo University, Kanagawa, Japan.
authors.forename: I
authors.initials: I
authors.lastname: Murakami
authors.forename: H
authors.initials: H
authors.lastname: Kosano
authors.forename: I
authors.initials: I
authors.lastname: Ogihara-Umeda
authors.forename: H
authors.initials: H
authors.lastname: Nishigori
authors.forename: S
authors.initials: S
authors.lastname: Uga
authors.forename: S
authors.initials: S
authors.lastname: Ishikawa
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D019328:Buthionine Sulfoximine / Q000494:pharmacology*; D002386:Cataract / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D002642:Chick Embryo; D005978:Glutathione / Q000378:metabolism; D006854:Hydrocortisone / Q000031:analogs & derivatives / Q000494:pharmacology; D007908:Lens, Crystalline / Q000187:drug effects* / Q000196:embryology / Q000378:metabolism / Q000648:ultrastructure; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008854:Microscopy, Electron
chemical_list: D000893:Anti-Inflammatory Agents; D008054:Lipid Peroxides; D019328:Buthionine Sulfoximine; D005978:Glutathione; C007133:hydrocortisone hemisuccinate; D006854:Hydrocortisone