A Mouse Model of Acute and Delayed Complications of Sulfur Mustard Analogue, 2-Chloroethyl Ethyl Sulfide

Document Type: Original Article

Authors

1 Immunoregulation Research Center , Shahed University< Tehran, Iran

2 Institute of Biochemistry and Biophysics, University of Tehran, Tehran, Iran.

3 Immunoregulation Research Center, Shahed University, Tehran, Iran.

4 Department of Biology, Faculty of Sciences, North Tehran Branch, Islamic Azad University, Tehran, Iran

5 Department of Anatomy Tissue and Pathology, School of Medicine, Shahed University, Tehran, Iran.

6 Department of Ophthalmology, Shahed University, Tehran, Iran.

7 Department of Social Medicine, School of Medicine, Fasa University of Medical Sciences, Fasa, Iran.

8 Department of Physiology, School of Medicine, Shahed University, Tehran, Iran

9 Department of Biostatistics and Epidemiology, Faculty of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.

Abstract

Background: Numerous studies have been conducted on humans, animals, and cell cultures exposed to Sulfur Mustard (SM). However, the precise mechanism and cause or long-term pattern of SM injuries are not well defined. There is no protocol available for treating people with severe eye, lung, and skin ailments. The current study aimed to develop an animal model of the acute and delayed complications of SM exposure.
Materials and Methods: Two strains of mice (BALB/c and C57BL/6), 6-8 weeks old at the onset of the study, were exposed to 2-Chloroethyl Ethyl Sulfide (CEES) (1-200 mg/kg) and solvents (Tyrode’s solution, Polyethylene Glycol 300, herbal oil) for a duration of 12 hours to 7 months. The administration route was Intraperitoneal (IP) injection. The mortality rate, signs, and apparent side effects were explored. At the end of the study, the mice’s lung, liver, and spleen tissues were extracted and fixed for future histopathological assessments.
Results: Tyrode’s solution and Polyethylene Glycol 300 solvents were not appropriate for the present research. Pathological features observed in BALB/c mice were better than the C57BL/6 mice. Overall, 10 mg/kg CEES was the most suitable dose, because it had the least mortality rate and demonstrated the most pathological findings, such as the infiltration of inflammatory cells and proliferation of fibroblasts and fibrotic tissue in the lung. Five months after the CEES administration, the delayed phase complications were studied.
Conclusion: The IP injection of 10 mg/kg CEES to BALB/c mice imitates short- and long-term complications of SM exposure in humans. This model is useful for preventing and treating SM exposure.

Keywords


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