Systemic disease as a model for development of the genetic ang cell terapy technologies

  • V. A. Kordium Institute of molecular biology and genetics of NAS of Ukraine, Ukraine, 03143, Kyiv, Akademika Zabolotnogo str., 150
  • D. M. Irodov Institute of molecular biology and genetics of NAS of Ukraine, Ukraine, 03143, Kyiv, Akademika Zabolotnogo str., 150
  • M. V. Drahulian Institute of molecular biology and genetics of NAS of Ukraine, Ukraine, 03143, Kyiv, Akademika Zabolotnogo str., 150
  • T. P. Gulko Institute of molecular biology and genetics of NAS of Ukraine, Ukraine, 03143, Kyiv, Akademika Zabolotnogo str., 150
  • P. V. Buchek Institute of molecular biology and genetics of NAS of Ukraine, Ukraine, 03143, Kyiv, Akademika Zabolotnogo str., 150
DOI: https://doi.org/10.7124/visnyk.utgis.14.1.540

Abstract

Aim. Injury using CCl4 triggers a cascade of reactions and conditions specific for systemic lesions caused by most external anthropogenic environmental factors. Conditions for obtaining a model of systemic injury of an organism have been developed for further performing of restoration technologies with the use of stem cells and cytokines. Methods. Tumor predisposed ICR mice were chosen as the model. Systemic damage was caused with multiple intraperitoneal administration of carbon tetrachloride. Results. The optimal doses and load duration, excess above which leads to irreversible changes in the body that are not amenable to self-healing, were found. Conclusions. The model obtained can be used to study various recovery technologies of systemic damages.

Keywords: systemic disease, model, carbon tetrachloride.

References

Recknagel R.O., Glende E.A., Dolak J.A., Waller L. Mechanisms of carbon tetrachloride toxicity. Pharmacol. Ther. 1989. Vol. 43(1). P. 39–54. doi: 10.1016/0163-7258(89)90050-8

McGregor D., Lang M. Carbon tetrachloride: genetic effects and other modes of action. Mutat. Res. 1996. Vol. 366(3). P. 81–95. doi: 10.1016/S0165-1110(96)00027-9

Manibusan M.K., Odin M., Eastmond D.A. Postulated carbon tetrachloride mode of action: a review. J. Environ. Sci. Health. C. Environ. Carcinog. Ecotoxicol. Rev. 2007. Vol. 25(3). P. 185–209. doi: 10.1080/10590500701569398

Kordium V. A., Shuvalova N. S. The concept of «origin» problem definition and attempt of analysis. Biopolym. Cell. 2013. Vol. 29(5). P. 428–440. doi: 10.7124/bc.000835

Das M., Boerma M., Goree J.R., Lavoie E.G., Fausther M., Gubrij I.B., Pangle A.K., Johnson L.G., Dranoff J.A. Pathological changes in pulmonary circulation in carbon tetrachloride (CCl4)-induced cirrhotic mice. PLoS One. 2014. Vol. 9(4). P. 39–43. doi: 10.1371/journal.pone.0096043

Constandinou C., Henderson N., Iredale J.P. Modeling liver fibrosis in rodents. Methods Mol. Med. 2005. Vol. 11. P. 37–50. doi: 10.1385/1-59259-940-0:237

Marques T.G., Chaib E., da Fonseca J.H., Lourenço A.C.R., Silva F.D., Ribeiro M.A.F., Galvao F.H.F., D’Albuquerque L.A.C. Review of experimental models for inducing hepatic cirrhosis by bile duct ligation and carbon tetrachloride injection. Acta Cir. Bras. 2012. 27(8). P. 89–94. doi: 10.1590/S0102-86502012000800013