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1.
Neurosciences. 2007; 12 (3): 191-197
in English | IMEMR | ID: emr-119531

ABSTRACT

To determine the protective effects of vitamin E against the damage inflicted by reactive oxygen species during toluene induced brain injury in rats using histopathological, biochemical, and behavioral parameters. Twenty-eight Wistar albino male rats were studied at Hacettepe University Faculty of Medicine Laboratories and Gazi University Faculty of Medicine Metabolism Laboratory in 2006. The rats were divided into 4 groups as follows: control group, toluene only treated group, both toluene and vitamin E treated group, and vitamin E only treated group. Histopathological changes were observed by hematoxylin and eosin staining and the TUNEL method. Serum lipid peroxide levels were measured by the thiobutyric acid method, and the open field test was used for behavioral testing. Our results show that edema between cells in the neuropil, particularly beneath the pia mater, and around congested blood vessels was observed in all groups with different severity. However the pyknotic neurons, in addition to infiltrative cells, were observed in the toluene group to be decreased by the administration of vitamin E, which can be confirmed by the euchromatic nucleated neurons in the cortex of both the toluene and vitamin E treated groups. The levels of malondialdehyde in each group also confirmed these histopathological findings. Significant differences were also found in the open field test between the groups. The differences between the toluene and vitamin E groups in biochemical, histologic, and behavioral examinations, supports the antioxidant protective role of vitamin E against the harmful effect of toluene on the brain


Subject(s)
Animals, Laboratory , Tocopherols , Rats, Wistar , Antioxidants , Brain/drug effects
2.
Saudi Medical Journal. 2005; 26 (3): 385-89
in English | IMEMR | ID: emr-74843

ABSTRACT

Tonsils [palatine and nasopharyngeal] are immunologically active tissues. Due to their anatomical location, they are considered to be the initial defense barrier against the antigens entering into the respiratory and gastrointestinal tract. Tonsils act against these antigens by producing and activating the lymphocytes, which are responsible for the immune response. In order to get information regarding the distribution of cell surface antigens on the epithelial, stromal and lymphoid cells of these organs, we performed immunohistochemical staining by using antibodies against CD99, CD71 and CD98 activation antigens. Tissue samples of 20 patients undergoing tonsillectomy and adenoidectomy who presented with recurrent tonsillitis and adenoid hypertrophy in the Otorhinolaryngology Department, Hacettepe University Medical Faculty Hospital, Ankara, Turkey in 2001, were obtained as partial tissue samples apart from pathological examination. Tissues were immunostained by the indirect immunoperoxidase method. Strong CD71 reactivity in macrophages was observed as an indicator of the active role of the macrophages in immunoresponse in the chronic inflammation reaction. The CD98 reactivity on the proliferative basal layer of epithelium was a usual finding, as its detection in epithelial neoplasms and proliferative states is well known. We did not observe any reactivity of CD98 in nasopharyngeal tonsil epithelium and lymphoid cells of either nasopharyngeal or palatine tonsils. The CD99 reactivity was observed in the T-cell dependent area. We determined some topographic difference in the expression of some activation antigens in the epithelial, stromal and lymphoid components of the palatine and nasopharyngeal tonsils. Further detailed studies directed to determine the role of these antigens in tonsils would help to understand the role of these molecules in inflammatory events


Subject(s)
Humans , Male , Female , Palatine Tonsil/immunology , Tonsillitis/immunology , Tonsillitis/pathology , Antigens, CD/immunology , Macrophages/immunology , Macrophages/ultrastructure , T-Lymphocytes/immunology , Tonsillectomy , Immunohistochemistry , Fusion Regulatory Protein-1
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