M.L. Blagonravov, M.M. Azova, V.A. Frolov

A lot of data concerning mechanisms of cardiomyocyte programmed cell death under different cardiovascular diseases has recently been published. It was found that the intensity of cardiomyocyte apoptosis increased in dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, myocarditis and other diffuse pathologic processes. Meanwhile the effect of toxic substances, in particular diphtheria toxin, on myocardial cell apoptotic activity is still poorly investigated. Thereupon we performed an experimental work to study intensity and initial pathways of cardiac cell apoptosis in diphtheria intoxication. Native diphtheria toxin dosed 0.3 DLM per 1 kg of animal body weight was singly introduced to rabbits intravenously. 1, 3 and 5 days later caspase 3 and caspase 8 activity in left and right ventricular myocardium was measured. Intact rabbits were used as a control. It was shown that on day 5 caspase 3 activity significantly increased in left ventricular myocardium and caspase 8 only had a tendency to elevation. Caspase 3 activity in right ventricular myocardium had no difference from control at any terms of investigation, therefore we didn-t evaluate caspase 8 activity. Thus diphtheria intoxication is accompanied by stimulation of the intrinsic (mitochondrial) apoptotic pathway. Evidently in the right ventricle diphtheria toxin suppresses its own apoptotic effect mediated with some metabolic disturbance by direct inactivation of caspase 3 and/or some other enzymes of caspase cascade.