ABSTRACT
We demonstrated selective activation of caspases in the thymus during heat shock, i.e. primary activation of initiator caspase 9 (but not caspase 8) and effector caspase 3 (but not caspase 6). Preadaptation to heat improved animal survival after heat shock and reduced heat shock-induced activation of both initiator and effector caspases. Hence, adaptation to heat produced an antiapoptotic effect, which was not selective towards receptor-dependent or mitochondrial pathway of the caspase cascade activation.
Subject(s)
Adaptation, Physiological , Caspases/metabolism , Thymus Gland/enzymology , Animals , Apoptosis , Cell Extracts , Enzyme Activation , Hot Temperature , Male , Rats , Rats, Wistar , Time FactorsABSTRACT
Accumulation of HSP70 stress proteins in the myocardium and blood content of nitrite/nitrate in August rats with modeled myocardial infarction surpassed these parameters in Wistar rats less resistant to cardiovascular disorders by 2-2.5 and 1.8 times, respectively. Our results suggest that various resistance of August and Wistar rats to myocardial infarction is related to genetically determined differences in the activity of HSP70 and nitric oxide systems.
Subject(s)
HSP70 Heat-Shock Proteins/biosynthesis , Myocardial Infarction/genetics , Myocardial Infarction/metabolism , Nitric Oxide/metabolism , Animals , Genetic Predisposition to Disease , Male , Myocardium/metabolism , Nitrates/blood , Nitric Oxide/biosynthesis , Nitrites/blood , Rats , Rats, Inbred Strains , Rats, Wistar , Species SpecificityABSTRACT
A lesser resistance against myocardial infarction (MI) in the Wistar rats as compared with the August rats was found to be combined with a greater stress-response and activation of the heart sympathetic regulation in the former rats. In the Wistar rats and not in August rats, an activation of hypothalamic noradrenaline (NA) system occurs as well as a greater "output" of the NA from sympathetic terminals in the myocardium. Accumulation of the HSP 70 stress-proteins in IM in the myocardium is nearly 2-2.5-fold lesser in the Wistar rats. Thereupon, different resistance against the IM in Wistar and August rats seems to be due to a genetically determine differences in intensity of the stress-response, activation of the heart sympathetic regulation in the IM, and production of the HSP 70 protective stress-proteins in the myocardium.
