الفهرس 
Fluoride
Clinical uses of trivalent chromiumOnly 14 pages are availabe for public view
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Abstract
Fluoride is an essential component for normal bone mineralization and formation of dental enamel. In excessive amounts, it may result in fluorosis. Fluorosis is a slow, progressive degenerative disorder that affects cerebellum as a part of the nervous system.
This study was done to investigate the possible toxic effect of low and high doses of sodium fluoride (NaF) on the cerebellar cortex of adult male albino rat for different periods of administration, and to detect the possible protective effect of chromium chloride (Cr Cl).
Sixty-five adult male albino rats were used in this study. They were divided into six groups; each group was subdivided into subgroups (a and b) which were treated for one and two months, respectively. Group 1 (control), Group II (treated with daily Cr Cl 300 µg/Kg), Group III (oral administration of daily NaF 6 mg/Kg), Group IV (oral administration of daily NaF 12mg/ Kg), Group V (oral co-administration of daily Cr Cl 300 µg/Kg and NaF 6 mg/Kg), Group VI (oral co-administration of daily Cr Cl 300 µg/Kg and NaF 12 mg/Kg). At the end of the experiment, the animals were sacrificed and the cerebella were dissected out and examined by light microscope with H&E, toluidine blue and Glees and Marseland’s technique. Immunohistochemical staining was done for glial fibrillary acidic protein (GFAP). The cerebella were also processed to be examined by transmission electron microscope.
The cerebellar cortex of NaF treated rats showed different degrees of neuro-degeneration. Light microscopic examination showed that the most affected layer was Purkinje cell layer. These degenerative changes were confirmed by statistical results. Increase in positively immunostained glial cells was observed in the molecular and granular layers. In severe toxicity glial cells extended to the Purkinje cell layer. Electron microscopic examination showed ultrastructural changes of Purkinje cell organelles as well as granule cells degeneration. Co-administration of Cr Cl ameliorated these toxic changes in different degrees.
Conclusion: Administration of NaF triggered different toxic changes in the histological architecture of the cerebellar cortex. Long duration of NaF administration induced more significant changes rather than the increase in the administrated dose. It was also observed that Cr Cl could provide partial protection against NaF induced toxicity.