Document Type : Original Article
Authors
1
Department of Human Anatomy and Embryology, Faculty of Medicine, Zagazig University, Egypt
2
ANATOMY DEPARTEMENT Zagazig university
3
Human Anatomy and Embryology Department, Faculty of Medicine, Cairo University, Egypt
4
Department of Human Anatomy and Embryology, Faculty of Medicine, Zagazig University, Egypt.
Abstract
Background: Furan, a cytotoxic chemical produced during thermal processing of foods, is an endocrine disruptor that induces injury of most endocrine glands. Objectives: To evaluate the effects of furan exposure on cytoarchitecture of the rat thyroid gland and to assess the potential protective role of selenium (Se). Methods: Twenty-four male Sprague Dawley rats were allocated into four groups and gavaged daily for 4 weeks. I (Control group) received corn oil, II (Se group) received selenium (1μg/100g bw/day), III (Furan group) received furan (40 mg/kg bw/day), and IV (Furan/Se group) received furan and Se simultaneously. Serology was performed and Paraffin sections of thyroid gland were processed for staining by H&E and Periodic Acid Schiff (PAS). Also, immunohistochemical study was carried out for detection of Fas protein and the proliferating cell nuclear antigen (PCNA). Moreover, morphometric analysis was performed. Results: Furan group exhibited discernible histopathological changes in the thyroid gland; outcomes associated with depleted thyrocolloid and decreased its mean area % and extensive immunoexpression of Fas and PCNA with increased their mean area %. In addition, furan group displayed increased serum malondialdehyde (MDA), interleukin-1 β (IL-1β), tumour necrosis factor alpha (TNF-α), and thyroid stimulating hormone (TSH) but serum reduced glutathione (GSH), glutathione peroxidase-1 (GPX-1) activity, and serum total T3, T4 were decreased. Co-supplementation of Se with furan partially ameliorated the histological, immunohistochemical and biochemical changes. Conclusions: Furan induced deleterious effects on rat thyroid gland that mediated mostly via induction of oxidative, inflammatory and Fas apoptotic pathways; resultants that were abrogated by Se.
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