Low Doses of Dimethylsulfoxide: Radioprotective and Cellular Properties

Sergey A. Bajinyan 1, Margarita H. Malakyan1, Ashot M. Dallakyan1, Artashes S. Poghosyan1, and Shiraz A. Markaryan2

1 Research Centre of Radiation Medicine and Burns, Ministry of Health, Yerevan, Republic of Armenia
2 Department Yerevan State University, Yerevan, Republic of Armenia

Corresponding author: Prof. Sergey A. Bajinyan, D.Sc.
    Research Centre of Radiation Medicine and Burns
    Ministry of Health of Armenia
    P.O. Box 25
    Davidashen, Yerevan, 370108
    Republic of Armenia
    Telephone: (374 1) 341 628, (374 1) 352 142
    Fax number: (374 1) 340 800
    E-mail address: bsergei@web.am

Key words:
Dimethylsulfoxide, radioprotection, erythrocytes, membrane potential, K+ outflow, lipid peroxidation, cytogenetics

CEJOEM 2002, Vol.8. No.4.: 322–329

Abstract:
In order to study the mechanisms of radioprotective activity of dimethylsulfoxide (DMSO), white inbred rats, controls and ones pretreated with DMSO (20 and 40 mg/kg), were exposed to total body irradiation with a single X-ray dose (5.7 Gy, LD100/30). Survival and the postirradiation mean lifetime were recorded. In different stages of radiation disease, the following measurements were made: level of membrane lipid peroxidation products, membrane potential, and passive K+ outflow from erythrocytes. In the surviving animals, analysis of the chromosomal apparatus of bone marrow cells (BMCs) was performed on the 30th postirradiation day. In the animals treated with 20 and 40 mg/kg DMSO, the survival amounted to 57.2% and 64.2%, respectively, in contrast to 0% in the control. The structural and functional changes of the erythrocyte membrane observed in the successive postirradiation stages of DMSO-pretreated rats appeared to be insufficient for total lethality. In the surviving animals, the analysis of the chromosomal apparatus of BMCs allows to suppose that definite genetic mechanisms underlie the radioprotective action of DMSO, which can, however, be diverse depending on the dose applied.

Received:  24 April 2002
Accepted:  6 December 2002
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