Browsing by Subject "Busulfan"

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    Microencephaly and microphthalmia in rat fetuses by busulfan
    (Murcia : F. Hernández, 2007) Furukawa, S.; Usuda, K.; Abe, M.; Ogawa, I.
    Microencephaly and microphthalmia in the embryos/fetuses from rats exposed to busulfan were histopathologically examined. Busulfan was intraperitoneally administered at 10 mg/kg on gestation days (Days) 12, 13 and 14, and then embryos/fetuses were harvested on Days 14.5, 15, 16 and 21. In the treated group on Day 21, all fetuses were small with reduced body weight, with microencephaly and microphthalmia. On Days 14.5, 15 and 16, apoptotic cells were increased in the neuroepithelium and the neural retina with a width reduction and a decrease in cell density, and the lens epithelial cells histopathologically. Mitotic inhibition was observed in the neuroepithelium, neural retina and equatorial zone of the lens. On Day 21, the cerebral cortex and the retina became markedly thinner. The lens fibers showed swollen, fragmentary and vacuolar formation in the cranial portion accompanied with small lens sizes. The anti-proliferative effects of busulfan brings about a lack of cell populations required for the normal organogenesis of the brain and eye, and leads to microencephaly and microphthalmia, featuring hypoplasia of cerebrum and hypoplasia of retina and lens with cataract, respectively
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    Ocular lesions induced in infant rats by busulfan
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Saito, Tsubasa; Ando, Ryo; Ohira, Toko; Hoshiya, Toru; Tamura, Kazutoshi
    Although busulfan, a bifunctional alkylating agent, is known to induce cataracts in infant rats, the full nature of busulfan-induced ocular lesions has not yet been shown. In order to clarify this point, 6-day-old rats were treated with a single dose of 20 mg/kg busulfan and the ocular tissue was histopathologically and immunohistochemically examined at 1, 2, 4, 7 and 12 days after treatment (DAT). As a result, in the nuclear layer (NL) of the peripheral retina, apoptotic cells significantly increased at 1 DAT and peaked at 2 DAT when cell proliferating activity was depressed. At 4 DAT, the NL showed wavy deformation with formation of rosette-like structures, and these changes progressed prominently at 12 DAT. In addition, a significant reduction in the retinal thickness due to decreased thickness of NL or inner NL was detected at 2 and 4 DAT. On the other hand, in the germinative zone of the lens equator, apoptotic lens epithelial cells significantly increased from 2 to 7 DAT, resulting in partial loss of lens epithelial cells at 7 and 12 DAT. At 12 DAT, prominent swelling and vacuolation of lens fibers were observed in the area from the equatorial zone to the posterior pole, indicating the development of cataract. The present results strongly suggest that prominent apoptosis in component cells was the initial and essential event underlying the developpment of busulfan-induced ocular lesions in infant rats.