ARTICLE INFO

Article Type

Original Research

Authors

Alamdar   L. (1 )
Ghazanfari   T. (* )
Salimi   H. (2 )






(* ) Immunoregulation Research Center, Shahed University, Tehran, Iran
(1 ) Immunoregulation Research Center, Shahed University, Tehran, Iran
(2 ) Zist Kavosh Iranian (IBRESCO), Tehran, Iran

Correspondence

Address: Immunoregulation Research Center, 4th Floor, Shahed University Research Centers Building, No. 1471, Corner of Mehr Alley, North Karegar Street, Enqelab Square, Tehran, Iran
Phone: +98 2188964792
Fax: +98 2188966310
tghazanfari@yahoo.com

Article History

Received:   July  26, 2014
Accepted:   August 19, 2014
ePublished:   February 19, 2015

ABSTRACT

Aims Mustard gas is an Alkalizing agent and inflammatory stimuli that were used as chemical weapon. Lung problems in people exposed to mustard gas is the major cause of morbidity and mortality in long-term. DNA damage is considered as one of the most important clinical lesions. Typically, apoptosis is occurred during development and aging and as a hemostatic mechanism for maintaining cell populations in tissues and also as a defence mechanism in immune system body reactions or when cells are suffered by toxic agents or illness. The aim of this study was to compare the rate of apoptosis in blood mononuclear cells of chemical victims 25 years after exposure to mustard gas and non-exposured people.
Materials & Methods This case control study was performed at 2014 on 10 veterans as case group selected by random sampling and 11 patients as control group selected by random sampling. 3mL of peripheral blood collected from both groups and gradient Faykl was used to isolation of mononuclear peripheral blood cells. After cells preparing, ELISA kit cell death was used to measure apoptosis. Data were analysed by student-T test.
Findings The mean incidence of apoptosis in control group was 0.533±0.168 and in case group was 0.345±0.116, which was not different significantly (p=0.39).
Conclusion Mustard gas in chronic phase (25 years after exposure) has no effect on apoptosis of peripheral blood mononuclear cells.


CITATION LINKS

[1]Ghabili K, Agutter PS, Ghanei M, Ansarin K, Panahi Y, Shoja MM. Sulfur mustard toxicity: History, chemistry, pharmacokinetics, and pharmacodynamics. Crit Rev Toxicol. 2011;41(5):384-403.
[2]Ghanei M, Aslani J, Khateri S, Hamadanizadeh K. Public health status of the civil population of Sardasht 15 years following large-scale wartime exposure to sulfur mustard. J Burns Surg Wound Care. 2003;2(7):7-18.
[3]Ghasemi H, Ghazanfari T, Yaraee R, Ghassemi-Broumand M, Soroush MR, Pourfarzam S, et al. Evaluation of relationship between the serum levels of inflammatory mediators and ocular injuries induced by sulfur mustard: Sardasht-Iran Cohort Study. Int Immunopharmacol. 2009;9(13-14):1494-8.
[4]Khateri S, Ghanei M, Keshavarz S, Soroush M, Haines D. Incidence of lung, eye, and skin lesions as late complications in 34,000 Iranians with wartime exposure to mustard agent. J Occup Environ Med. 2003;45(11):1136-43.
[5]Aragizadeh H, Soroush M-R, Javadi M-A, Azizi F, Ghasemi H, Shams J, et al. Sardasht-Iran cohort study of chemical warfare victims: Design and methods. Arch Iran Med. 2009;12(1):5-14.
[6]Paromov V, Suntres Z, Smith M, Stone WL. Sulfur mustard toxicity following dermal exposure: Role of oxidative stress, and antioxidant therapy. J Burns Wounds. 2007;7:e7.
[7]Gao X, Ray R, Xiao Y, Ray P. Suppression of inducible nitric oxide synthase expression and nitric oxide production by macrolide antibiotics in sulfur mustard-exposed airway epithelial cells. Basic Clin Pharmacol Toxicol. 2008;103(3):255-61.
[8]Lodhi IJ, Sweeney JF, Clift RE, Hinshaw DB. Nuclear dependence of sulfur mustard-mediated cell death. Toxicol Appl Pharmacol. 2001;170(1):69-77.
[9]Lawley PD, Brookes P. Interstrand cross-linking of DNA by difunctional alkylating agents. J Mol Biol. 1967;25(1):143-60.
[10]Ludlum DB, Tong WP, Mehta JR, Kirk MC, Papimeister B. Formation of O6-ethylthioethyldeoxyguanosine from the reaction of chloroethyl ethyl sulfide with deoxyguanosine. Cancer Res. 1984;44(12 Part 1):5698-701.
[11]Ludlum DB, Kent S, Mehta JR. Formation of O6-ethylthioethylguanine in DNA by reaction with the sulfur mustard, chloroethyl sulfide, and its apparent lack of repair by O6-alkylguanine-DNA alkyltransferase. Carcinogenesis. 1986;7(7):1203-6.
[12]Dronkert ML, Kanaar R. Repair of DNA interstrand cross-links. Mutat Res Repair. 2001;486(4):217-47.
[13]Elmore S. Apoptosis: A review of programmed cell death. Toxicol Pathol. 2007;35(4):495-516.
[14]Pirzad G, Jafari M, Tavana S, Sadrayee H, Ghavami S, Shajiei A, et al. The role of fas-fasl signaling pathway in induction of apoptosis in patients with sulfur mustard-induced chronic bronchiolitis. J Toxicol. 2010. Available from: http://dx.doi.org/10.1155/2010/373612.
[15]Ray R, Simbulan-Rosenthal CM, Keyser BM, Benton B, Anderson D, Holmes W, et al. Sulfur mustard induces apoptosis in lung epithelial cells via a caspase amplification loop. Toxicology. 2010;271(3):94-9.
[16]Debiak M, Kehe K, Bürkle A. Role of poly (ADP-ribose) polymerase in sulfur mustard toxicity. Toxicology. 2009;263(1):20-5.
[17]Rosenthal DS, Simbulan-Rosenthal CM, Iyer S, Spoonde A, Smith W, Ray R, et al. Sulfur Mustard Induces Markers of Terminal Differentiation and Apoptosis in Keratinocytes Via a Ca2+-Calmodulin and Caspase-Dependent Pathway. J Invest Dermatol. 1998;111(1):64-71.
[18]Dabrowska MI, Becks LL, Lelli Jr JL, Levee MG, Hinshaw DB. Sulfur mustard induces apoptosis and necrosis in endothelial cells. ToxicolApplPharmacol. 1996;141(2):568-83.
[19]Mol MA, van de Ruit A-MB, Kluivers A. NAD+ levels and glucose uptake of cultured human epidermal cells exposed to sulfur mustard. Toxicol Appl Pharmacol. 1989;98(1):159-65.
[20]Hinshaw DB, Lodhi IJ, Hurley LL, Atkins KB, Dabrowska MI. Activation of Poly [ADP-Ribose] Polymerase in Endothelial Cells and Keratinocytes: Role in aninVitroModel of Sulfur Mustard-Mediated Vesication. ToxicolApplPharmacol. 1999;156(1):17-29.
[21]Roche Diagnostics. Cell death detection elisa plus [Internet]. [Cited: 2014 May 3]. Available from: https://www.google.com/webhp?hl=en&authuser=0#authuser=0&hl=en&q=cell+death+detection+elisa+plus.
[22]Etezad-Razavi M, Mahmoudi M, Hefazi M, Balali-Mood M. Delayed ocular complications of mustard gas poisoning and the relationship with respiratory and cutaneous complications. Clin Experiment Ophthalmol. 2006;34(4):342-6.
[23]Keyser BM, Andres DK, Nealley E, Holmes WW, Benton B, Paradiso D, et al. Postexposure application of Fas Receptor Small-Interfering RNA to Suppress Sulfur Mustard-Induced Apoptosis in Human Airway Epithelial Cells: Implication for a Therapeutic Approach. J Pharmacol Exp Ther. 2013;344(1):308-16.
[24]Behravan E, Moallem SA, Khateri S, Maraghi E, Jowsey P, Blain PG, et al. Deoxyribonucleic acid damage in Iranian veterans 25 years after wartime exposure to sulfur mustard. J Res Med Sci Off J Isfahan Univ Med Sci. 2013;18(3):239.
[25]Roshanzamir T, Mirkheshti N, Ghassami F, Moghadam NA, Ali S. Bcl-2 Protein Expression in Pulmonary Specimens of Sulfur Mustard Victims. Tanaffos. 2008;7(1):25-31.