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  • 1
    ISSN: 1432-0533
    Schlagwort(e): Key words 2,5-Di(tert-butyl)-1,4-hydroquinone (DTBHQ) ; Wistar rat ; Motor endplate ; Lumbrical ¶muscle ; Neurocalcin
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract A time-course study of ultrastructural changes and immunoelectron microscopic localization of neurocalcin was performed on motor endplates of the lumbrical muscles of female Wistar rats given a single oral administration of 2,5-di(tert-butyl)-1,4-hydroquinone (DTBHQ) at a dose of 120 mg/kg. Toxic signs such as salivation and muscle weakness of the hind legs appeared from 3 h after DTBHQ administration. No remarkable macroscopic or light microscopic changes were noted in the lumbrical muscles of the treated rats. At the ultrastructural level, neurotoxicity characterized by a decreases or loss of synaptic vesicles and mitochondria was observed after 24 h and at the 1-week time point, nerve endings had disappeared in some of the motor endplates, while many neurite nerve endings suggestive of early stage regeneration were apparent. After 6 weeks, newly formed reinnervated endplates were observed. Immunoelectron microscopically, the synaptic vesicle membranes were heavily labeled for neurocalcin in the control rats, but not at 24 h after DTBHQ treatment. Synaptic vesicle membranes in the DTBHQ group were weakly labeled at 1 week, but strongly at 6 weeks. The results strongly suggest that DTBHQ targets the motor endplates in the rat lumbrical muscles, causing depletion of neurocalcin in the synaptic vesicles followed by their loss.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1432-0738
    Schlagwort(e): Key words Nitrobenzene ; Apoptosis ; Testicular toxicity
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Nitrobenezene (NB) produces germ cell degeneration, especially of spermatocytes in rats. To examine the possible involvement of apoptosis in this process, the extent and nature of nuclear DNA fragmentation after NB dosing were assessed using both terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) and DNA gel electrophoresis, in addition to conventional histological and electron microscopic procedures. Adult Sprague Dawley rats were treated with a single oral dose of NB (250 mg/kg) and euthanized subsequently at 6, 12, and 24 h and 2, 3, 5, and 7 days. The earliest morphological signs of germ cell degeneration in testes were found in pachytene spermatocytes 24 h after dosing. Electron micrographs of degenerating spermatocytes showed marked nuclear chromatin condensation at the nuclear periphery and crowding of cytoplasmic constituents, which are characteristic of apoptosis. Coincident with the appearance of such morphological changes, degenerating spermatocytes contained fragmented DNA as revealed by TUNEL. The presence of DNA laddering, a hallmark of apoptosis on gel electrophoresis, was first apparent and most prominent at 24 h, gradually becoming less detectable. No such changes were observed up to 12 h after dosing or in control animals. These results demonstrated unequivocal involvement of apoptosis in the induction of germ cell degeneration caused by NB.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    ISSN: 1432-0738
    Schlagwort(e): Key words Doxorubicin ; Apoptosis ; Testicular toxicity
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract To clarify whether apoptosis is involved in doxorubicin (DXR)-induced testicular toxicity and to identify the target germ cell type, adult Sprague-Dawley rats were treated with a single intravenous dose of DXR (8 or 12 mg/kg) and euthanized at 3, 6, 12, 24, and 48 h subsequently. Histologically, germ cell degeneration was first found 6 h after dosing in meiotically dividing spermatocytes and early round spermatids of seminiferous tubules at stage I, and subsequently observed in spermatogonia at stages I–VI showing ultrastructural characteristics of apoptosis. Coincident with the appearance of morphological changes, degenerating germ cells were shown to be undergoing apoptosis as revealed by in situ terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). The frequency of TUNEL-labeled germ cells increased in a stage- and cell type-specific manner, the peak of frequency gradually progressing from stage I of seminiferous tubules to later stages with time after dosing, suggesting that the damaged germ cells, especially spermatogonia, gradually underwent the processes leading to apoptosis. DNA laddering on gel electrophoresis was apparent 24 and 48 h after dosing. The results demonstrate that apoptosis plays an important role in the induction of testicular toxicity caused by DXR with meiotically dividing spermatocytes and type A and intermediate spermatogonia as highly vulnerable target cells.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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