The review concerns a number of basic molecular pathways that
play a crucial role in perception, transmission, and modulation of
the stress signals, and mediate the adaptation of the vital
processes in the cardiovascular system (CVS). These highly
complex systems for intracellular transfer of information include
stress hormones and their receptors, stress-activated
phosphoprotein kinases, stress-activated heat shock proteins,
and antioxidant enzymes maintaining oxidoreductive homeostasis
of the CVS. Failure to compensate for the deleterious effects of
stress may result in the development of different
pathophysiological states of the CVS, such as ischemia,
hypertension, atherosclerosis and infarction. Stress-induced
dysbalance in each of the CVS molecular signaling systems and
their contribution to the CVS malfunctioning is reviewed. The
general picture of the molecular mechanisms of the stressinduced pathophysiology in the CVS pointed out the importance
of stress duration and intensity as etiological factors, and
suggested that future studies should be complemented by the
careful insights into the individual factors of susceptibility to
stress, prophylactic effects of 'healthy' life styles and beneficial
action of antioxidant-rich nutrition.
In order to examine if differences in activity and inducibility of antioxidative enzymes in rat cerebral cortex and hippocampus are underlying their different sensitivity to radiation, we exposed four-day-old female Wistar rats to cranial radiation of 3 Gy of gamma-rays. After isolation of hippocampus and cortex 1 h or 24 h following exposure, activities of copper-zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD) and catalase (CAT) were measured and compared to unirradiated controls. MnSOD protein levels were determined by SDS-PAGE electrophoresis and Western blot analysis. Our results showed that CuZnSOD activity in hippocampus and cortex was significantly decreased 1 h and 24 h after irradiation with 3 Gy of gamma-rays. MnSOD activity in both brain regions was also decreased 1 h after irradiation. 24 h following exposure, manganese SOD activity in hippocampus almost achieved control values, while in cortex it significantly exceeded the activity of the relevant controls. CAT activity in hippocampus and cortex remained stable 1 h, as well as 24 h after irradiation with 3 Gy of gamma-rays. MnSOD protein level in hippocampus and cortex decreased 1 h after irradiation with 3 Gy of gamma-rays. 24 h after exposure, MnSOD protein level in cortex was similar to control values, while in hippocampus it was still significantly decreased. We have concluded that regional differences in MnSOD radioinducibility are regulated at the level of protein synthesis, and that they represent one of the main reasons for region-specific radiosensitivity of the brain.
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