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Hammam Sousse, Tunisia

Tebourbi O.,University of Carthage | Hallegue D.,University of Carthage | Yacoubi M.T.,Laboratory of Pathologic Anatomy | Sakly M.,University of Carthage | Rhouma K.B.,University of Carthage
Environmental Toxicology and Pharmacology | Year: 2010

The purpose of this study is to assess the effect of p,p′-DDT on thyroid activity of male Wistar rats. Pesticide was administered intraperitoneally (i.p.) for 10 consecutive days at doses of 50 and 100mg/kg/day. At the end of the treatment, the endpoints examined included serum total levels of triiodothyronine (T3), total thyroxine (T4), and thyroid stimulating hormone (TSH). Thyroid gland histopathology and tissue metabolism of thyroid hormone (T4 UDP-glucuronyltransferase UDP-GT and 5′-deiodinases) were determined. DDT treatment altered thyroid function namely by increasing hepatic excretion of T4 glucuronide. At the dose of 50mg/kg it decreased T4 circulating levels and increased thyroid 5′-deiodinase type I (5′-D-I) and brown adipose tissue (BAT) 5′-deiodinase type II (5′-D-II) activities but it did not affect liver 5′-D-I activity which might contribute to the maintenance of the serum T3 level. Treatment with 100mgDDT/kg decreased serum thyroid hormone concentration and tissue 5′-D-I activity without affecting BAT 5′-D-II activity. Gland histomorphological analysis showed hyperplasia and squamous metaplasia with abundant colloid. These observations associated to the elevated serum TSH levels and gland hypertrophy suggest that DDT exposure induced an hypothyroidism state with a colloid goiter in rats. © 2010 Elsevier B.V. Source


Tlili M.,University of Carthage | Tlili M.,French Institute of Health and Medical Research | Tlili M.,Institut Universitaire de France | Tlili M.,University of Rouen | And 11 more authors.
Oxidative Medicine and Cellular Longevity | Year: 2015

The rate of atmospheric vanadium is constantly increasing due to fossil fuel combustion. This environmental pollution favours vanadium exposure in particular to its vanadate form, causing occupational bronchial asthma and bronchitis. Based on the well admitted bronchodilator properties of the pituitary adenylate cyclase-activating polypeptide (PACAP), we investigated the ability of this neuropeptide to reverse the vanadate-induced airway hyperresponsiveness in rats. Exposure to ammonium metavanadate aerosols (5 mg/m3/h) for 15 minutes induced 4 hours later an array of pathophysiological events, including increase of bronchial resistance and histological alterations, activation of proinflammatory alveolar macrophages, and increased oxidative stress status. Powerfully, PACAP inhalation (0.1 mM) for 10 minutes alleviated many of these deleterious effects as demonstrated by a decrease of bronchial resistance and histological restoration. PACAP reduced the level of expression of mRNA encoding inflammatory chemokines (MIP-1α, MIP-2, and KC) and cytokines (IL-1α and TNF-α) in alveolar macrophages and improved the antioxidant status. PACAP reverses the vanadate-induced airway hyperresponsiveness not only through its bronchodilator activity but also by counteracting the proinflammatory and prooxidative effects of the metal. Then, the development of stable analogs of PACAP could represent a promising therapeutic alternative for the treatment of inflammatory respiratory disorders. © 2015 Mounira Tlili et al. Source


Papaoiconomou E.,National and Kapodistrian University of Athens | Lymperi M.,National and Kapodistrian University of Athens | Petraki C.,Laboratory of Pathologic Anatomy | Philippou A.,National and Kapodistrian University of Athens | And 6 more authors.
Anticancer Research | Year: 2014

Background: Numerous studies have shown that the Kiss-1 gene countervails the metastatic aptitude of several cancer cell lines and solid-tumor neoplasias. However, there still remains ambiguity regarding its role in breast cancer and literature has arisen asserting that Kiss-1 expression may be linked to an aggressive phenotype and malignant progression. Herein, we investigated the protein expression of Kiss-1 and its receptor GPR54 in breast cancer tissues compared to non-cancerous mammary tissues. Materials and Methods: Paraffin-fixed cancer tissues from 43 women with resected breast adenocarcinomas and 11 specimens derived from women suffering from fibrocystic disease, serving as controls, were immunostained with Kiss- 1 and GPR54 antibodies. Results: Kiss-1 and GPR54 protein expression levels were significantly higher in breast cancer compared to fibrocystic tissues (p0.05). No significant correlation was established between Kiss-1 or GRP54 expression and tumor grade, tumor size, lymph node positivity, histological type or ER status. Kiss-1 expression significantly and positively correlated with GPR54 expression in both breast cancer and fibrocystic disease specimens. Conclusion: Kiss-1/GPR54 expression was found to be significantly higher in breast cancer compared to nonmalignant mammary tissues. Source

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