Document Type : Original articles

Authors

1 Department of Oral Diagnosis, College of Dentistry, Tikrit University, Tkrit, Iraq.

2 Department of Basic Sciences , College of Dentistry, Tikrit University, Tkrit, Iraq.

3 Department of Pathology , College of Veterinary Medicine, Tikrit University, Tkrit, Iraq.

4 Department of Nursing Dentistry, Technical Institute of Sulaimani, Polytechnic University of Sulaimani, Sulaimani, Iraq

Abstract

Background: The functional deterioration of salivary glands is a consequence of a wide range of factors and significantly interfered with life quality. Desloratadine (an antihistamine) is among the drugs listed to cause dry mouth; however, its effect on major salivary gland tissues has not been well studied.
Objectives: To evaluate the effects of desloratadine treatment on parotid gland tissues, histological features, and their impact on serum oxidative and antioxidant markers. 
Materials and Methods: Thirty rats were used in this study. They were divided into three groups (each containing ten rats). Group A: control rats. Group B and C have received desloratadine at dose 0.142 and 0.245 mg/kg of body weight respectively for three weeks. After three weeks, serum levels of sialic acid, malondialdehyde, catalase, lactate dehydrogenase, superoxide dismutase, creatin kinase, and glutathione were estimated for three groups. Then, animals were sacrificed and five µm formalin-fixed paraffin-embedded tissue sections were prepared routinely from parotid glands for histological evaluation under light microscope.
Results: The histological evaluation of salivary gland tissues in both treated-groups was revealed a remarkable cytoplasmic vacuolization, atrophy, and degranulation in acinic cells. The serous acinar cells were showed autolysis and nuclear changes (pyknosis, karyorrhexis, and karyolysis). There was an increase in the interstitial spaces between each parenchymal element associated with few mononuclear cell infiltrations. The intra-lobular ducts were reduced in size and were indistinct throughout lobes. The severe changes were associated with higher desloratadine dose. Regarding biochemical analysis, the treated-groups had significantly increased serum levels of malondialdehyde, sialic acid, lactate dehydrogenase and creatin kinase, and significantly reduced serum levels of superoxide dismutase, catalase, and glutathione. 
Conclusions: Desloratadine administration produces noticeable histological changes in a dose-dependent manner associated with increased oxidative stress markers and decreased antioxidative activity. 

Keywords

Main Subjects

[1]      M. W. J. Dodds, D. A. Johnson, and C.-K. Yeh, “Health benefits of saliva: a review,” J. Dent., vol. 33, no. 3, pp. 223–233, 2005.
[2]      B. W. Neville, D. D. Damm, C. M. Allen, and J. E. Bouquot, “Oral and maxillofacial pathology connective tissue lesion,” Connect. tissue lesion. 2nd ed. Saunders Philadelphia, p. 482, 2002.
[3]      M. Lenander-Lumikari and V. Loimaranta, “Saliva and dental caries,” Adv. Dent. Res., vol. 14, no. 1, pp. 40–47, 2000.
[4]      E. W. Odell, Cawson’s essentials of oral pathology and oral medicine e-book. Elsevier Health Sciences, 2017.
[5]      I. Sadowska-Woda, B. Sychta, M. Rachel, and E. Bieszczad-Bedrejczuk, “Protective effect of desloratadine against oxidative stress in human erythrocytes in vitro,” Environ. Toxicol. Pharmacol., vol. 30, no. 2, pp. 141–146, 2010.
[6]      P. Devillier, N. Roche, and C. Faisy, “Clinical pharmacokinetics and pharmacodynamics of desloratadine, fexofenadine and levocetirizine,” Clin. Pharmacokinet., vol. 47, no. 4, pp. 217–230, 2008.
[7]      D. Kim and J. N. Baraniuk, “Neural aspects of allergic rhinitis,” Curr. Opin. Otolaryngol. Head Neck Surg., vol. 15, no. 4, pp. 268–273, 2007.
[8]      A. Tatar, S. N. Parlak, M. Yayla, R. A. Ugan, E. Polat, and Z. Halici, “Effects of allergic rhinitis and desloratadine on the submandibular gland in a rat allergy model,” in International Forum of Allergy & Rhinology, 2015, vol. 5, no. 12, pp. 1164–1169.
[9]      G. Kroemer and B. Levine, “Autophagic cell death: the story of a misnomer,” Nat. Rev. Mol. cell Biol., vol. 9, no. 12, pp. 1004–1010, 2008.
[10]    D. Ekuni et al., “Imbalance of oxidative/anti-oxidative status induced by periodontitis is involved in apoptosis of rat submandibular glands,” Arch. Oral Biol., vol. 55, no. 2, pp. 170–176, 2010.
[11]    G. Şimşek et al., “Protective effects of resveratrol on salivary gland damage induced by total body irradiation in rats,” Laryngoscope, vol. 122, no. 12, pp. 2743–2748, 2012.
[12]    G. Boraks, F. S. Tampelini, K. F. Pereira, and R. P. Chopard, “Effect of ionizing radiation on rat parotid gland,” Braz. Dent. J., vol. 19, no. 1, pp. 73–76, 2008.
[13]    L. R. Azevedo-Alanis, E. de S. Tolentino, G. F. de ASSIS, T. M. Cestari, V. S. Lara, and J. H. Damante, “Acinar autolysis and mucous extravasation in human sublingual glands: a microscopic postmortem study,” J. Appl. Oral Sci., vol. 23, no. 5, pp. 459–466, 2015.
[14]    S. SYRJÄNEN, “Age-related changes in structure of labial minor salivary glands,” Age Ageing, vol. 13, no. 3, pp. 159–165, 1984.
[15]    D. Dayan, M. Vered, S. Sivor, Y. Hiss, and A. Buchner, “Age-related changes in proliferative markers in labial salivary glands: a study of argyrophilic nucleolar organizer regions (AgNORs) and Ki-67,” Exp. Gerontol., vol. 37, no. 6, pp. 841–850, 2002.
[16]    J.-S. Choi, I. S. Park, S. Kim, J.-Y. Lim, and Y.-M. Kim, “Analysis of age-related changes in the functional morphologies of salivary glands in mice,” Arch. Oral Biol., vol. 58, no. 11, pp. 1635–1642, 2013.
[17]    H. Prasad, V. Ramesh, and P. D. Balamurali, “Morphologic and cytomorphometric analysis of exfoliated buccal mucosal cells in diabetes patients,” J. Cytol. Acad. Cytol., vol. 27, no. 4, p. 113, 2010.
[18]    N. J. Holbrook and S. Ikeyama, “Age-related decline in cellular response to oxidative stress: links to growth factor signaling pathways with common defects,” Biochem. Pharmacol., vol. 64, no. 5–6, pp. 999–1005, 2002.
[19]    J. Scott, “Quantitative age changes in the histological structure of human submandibular salivary glands,” Arch. Oral Biol., vol. 22, no. 3, pp. 221–227, 1977.
[20]    J. P. Prestifilippo et al., “Histamine modulates salivary secretion and diminishes the progression of periodontal disease in rat experimental periodontitis,” Inflamm. Res., vol. 61, no. 5, pp. 455–464, 2012.
[21]    V. A. Medina et al., “Histamine prevents functional and morphological alterations of submandibular glands induced by ionising radiation,” Int. J. Radiat. Biol., vol. 87, no. 3, pp. 284–292, 2011.
[22]    E. R. Sarhat, “Altered serum marker of thyroid profile and antioxidant enzymes in individuals Alzheimer’s disease,” Int. Res. J. Pharm, vol. 10, no. 1, pp. 56–60, 2019.
[23]    E. R. Sarhat, I. J. Mohammed, N. Y. Mohammed, B. S. Khairy, and G. F. Hassan, “Evaluation of Salivary Oxidative Stress Marker (Lipid Peroxidation), and Non-Enzymatic Antioxidants (Vitamin C and Vitamin E) in Patients with Acute Myocardial Infarction,” Tikrit J. Dent. Sci., vol. 7, no. 1, pp. 20–26, 2019.
[24]    E. R. Sarhat, S. A. Wadi, and A. R. Mahmood, “Effect of Ethanolic Extraction of Moringa oleifera on Paraoxonase and Arylesterase enzyme activity in High Fat Diet-induced Obesity in Rats,” Res. J. Pharm. Technol., vol. 11, no. 10, pp. 4601–4604, 2018.
[25]    R. S. Entedhar, “Effect of Ginger on the activity of some antioxidant enzymes (Superoxide dismutase, and Catalase) of Alloxan Experimental Induced-Diabetic Rabbits,” Al-Mustansiriyah J. Sci, vol. 22, no. 5, pp. 192–200, 2011.
[26]    E. R. Sarhat, B. A. Abdullah, and S. A. Wadi, “Experimental study of effect of ginger ethanolic extract on oxidative stress in alloxan induced-diabetic rabbits,” in 3rd Scientific Conference—College of Veterinary Medicine—University of Tikrit, 2016, pp. 2–3.
[27]    K. G. W. E. R. Sarhat and T. H. Jabir, “Assessment of Melatonin and Oxidant-Antioxidant Markers in Infertile Men in Thi-Qar Province,” Indian J. Forensic Med. Toxicol., vol. 13, no. 4, pp. 1500–1504, 2019.
[28]    H. A. Takhtfooladi, M. A. Takhtfooladi, P. Karimi, H. A. Asl, and S. Z. M. N. Mobarakeh, “Influence of tramadol on ischemia–reperfusion injury of rats’ skeletal muscle,” Int. J. Surg., vol. 12, no. 9, pp. 963–968, 2014.
[29]    A. S. Kini et al., “Correlation of postpercutaneous coronary intervention creatine kinase-MB and troponin I elevation in predicting mid-term mortality,” Am. J. Cardiol., vol. 93, no. 1, pp. 18–23, 2004.
[30]    E. R. Sarhat, M. M. Y. Al-Anzy, M. S. Ahmeid, and T. R. Sarhat, “Characteristic Abnormalities in Serum Biochemistry during Congestive heart failure,” Med. J. Tikrit Univ., vol. 24, no. 1, pp. 69–77, 2018.