Toxic cardiac effect of cobalt chloride excessive chronic consumption in male Wistar rats

Tatiana P. Sataieva, Igor V. Zadnipryany, Walery Zukow



Cobalt is widespread in the natural environment and can be formed as an effect of anthropogenic activity. The ionic cobalt can be transported by blood in the body, causing adverse effects by the generation of reactive oxygen species. The aim of this research was to describe the changes of myocardial cells during experimental cobalt induced cardiomyopathy. Summarizing the in vivo experiments, it can be stated that severe histotoxic cardiomyopathy occurred in male rats treated with cobalt chloride. Long-term oral administration of cobalt resulted in diminished dietary intake and growth inhibition in the exposed rats compared to the control group. The primary morphological alteration of cardiomyocytes is mitochondrial damage that possibly reflects an enzymatic block of oxidative decarboxylation. Due to that myofibrils of the myocardial cells were affected highlighting that the main cause of myofibril reduction could be a lower oxygen intake in the perinuclear area. The reduction of the contractile support of myocardial cells can explain the possible myocardial dysfunction. Knowing structural changes in cardiomyocytes could explain the pathophysiology of the disease and allow a correct therapeutic approach.


cobalt chloride; myocardium; cardiomyocyte; mitochondria; histotoxic hypoxia; rats

Full Text:



Afridi H.I., Kazi T.G., Kazi N., Kandhro G.A., Baig J.A., Jamali M.K., Arain M.B., Shah A.Q., Shah F., Khan S. & Kolachi N.F., 2011, Association of environmental toxic elements in biological samples of myocardial infarction patients at different stages. Biol. Trace. Elem. Res. 141: 26–40. (PMID: 20480400 doi: 10.1007/s12011-010-8713-2).

Alexander C.S., 1968, The syndrome of cobalt-beer cardiomyopathy including ultrastructural changes on biopsy. J. Lab. Clin. Med. 72: 850.

Battaglia V., Compagnone A., Bandino A., Bragadin M., Rossi C.A., Zanetti F., Colombatto S., Grillo M.A. & Toninello A., 2009, Cobalt induces oxidative stress in isolated liver mitochondria responsible for permeability transition and intrinsicapoptosis in hepatocyte primary cultures. Int. J. Biochem. Cell Biol. 41: 586–594. (PMID: 18708157 doi: 10.1016/j.biocel.2008.07.012).

Bruick R.K., 2003, Oxygen sensing in the hypoxic response pathway: regulation of the hypoxia-inducible transcription factor. Genes Dev. 17: 2614–2623. (PMID: 14597660 doi: 10.1101/gad.1145503).

Czarnek K., Terpiłowska S. & Siwicki A.K., 2015, Selected aspects of the action of cobalt ions in the human body. Cent. Eur. J. Immunol. 40(2): 236-42. (PMID: 26557039 PMCID: PMC4637398 doi: 10.5114/ceji.2015.52837).

Edel J., Pozzi G., Sabbioni E. Pietra R. & Devos S., 1994, Metabolic and toxicological studies on cobalt. Sci. Total Environ. 150: 233–244.

Goldoni M., Catalani S., De Palma G. Manini P., Acampa O., Corradi M., Bergonzi R. Apostoli P. & Mutti A., 2004, Exhaled breath condensate as a suitable matrix to assess lung dose and effects in workers exposed to cobalt and tungsten. Environ. Health Perspect. 112: 1293–1298. (PMID: 15345342 PMCID: PMC1247519 doi: 10.1289/ehp.7108).

Hibbs R.G., Black W.C., 1965, Electron microscopy of post-mortem changes in the rat myocardium. The Anatomical Record 147(2): 261-72. (PMID: 14065938 doi: 10.1002/ar.1091470209).

Huy N.D., Morin P.J., Mohiuddin S.M. & Morin Y., 1973, Acute effects of cobalt on cardiac metabolism and mechanical performance. Can. J. Physiol. Pharmacol. 51: 46–51.

Karovic O., Tonazzini I., Robola N., Edstrцm E., Lцvdahl C., Fredholm B.B. & Darй E., 2007, Toxic effects of cobalt in primary cultures of mouse astrocytes. Similarities with hypoxia and role of HIF-1alpha. Biochem Pharmacol. 73: 694–708. (PMID: 17169330 doi: 10.1016/j.bcp.2006.11.008).

Lison D., De Boeck M., Verougstraete V. & Kirsch-Volders M., 2001, Update on the genotoxicity and carcinogenicity of cobalt compounds. Occup Environ Med. 58: 619–625. PMID: 11555681 PMCID: PMC1740056

Malard V., Berenguer F., Pratt O. Ruat S., Steinmetz G. & Quemeneur E., 2007, Global gene expression profiling in human lung cells exposed to cobalt. BMS Genomics. 8: 147–164. (PMID: 17553155 PMCID: PMC1904204 doi: 10.1186/1471-2164-8-147).

McKinney J. & Rogers R., 1992, Metal bioavailability. Environ. Sci. Technol. 26(7): 1298–1299.

National Research Council, 1985, Guide for the Care and Use of Laboratory Animals, 6th ed. NIH Pub. No. 86-23. Washington, DC: US Department of Health and Human Services.

Nemery B., Lewis C.P.L., & Demedts M., 1994, Cobalt and possible oxidant-mediated toxicity. Sci. Total Environ. 150: 57–64.

Ortega R., Bresson C., Fraysse A., Sandre C., Devès G., Gombert C., Tabarant M., Bleuet P., Seznec H., Simionovici A., Moretto P., & Moulin C., 2009, Cobalt distribution in keratinocyte cells indicates nuclear and perinuclear accumulation and interaction with magnesium and zinc homeostasis. Toxicol. Lett. 188:26–32. (PMID: 19433266 doi: 10.1016/j.toxlet.2009.02.024).

Patel E., Lynch Ch., Ruff V. & Reynolds M., 2012, Co-exposure to nickel and cobalt chloride enhances cytotoxicity and oxidative stress in human lung epithelial cells. Toxicol. Appl. Pharmacol. 258: 367–375. (PMID: 22172632 doi: 10.1016/j.taap.2011.11.019).

Pulido M.D. & Parrish A.R., 2003, Metal-induced apoptosis: mechanisms. Mutat Res. 533: 227–241. (PMID: 14643423).

Simonsen L.O., Harbak H. & Bennekou P., 2012, Cobalt metabolism and toxicology – a brief update. Sci Total Environ. 432: 210–215. (PMID: 22732165 doi: 10.1016/j.scitotenv.2012.06.009).

Zadnipryany I.V., Tretiakova O.S., Sataieva T.P. & Zukow W., 2017, Experimental ‏review ‏of ‏cobalt ‏induced cardiomyopathy. Russian Open Medical Journal 6(1): 1-4. (

Partnerzy platformy czasopism