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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.

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