ENDOGENOUS ANTIOXIDANT CHANGES IN THE MYOCARDIUM IN RESPONSE TO ACUTEAND CHRONIC STRESS CONDITIONS

Oxygen is a diradical and because of its unique electronic configurati on, it has the potential to form strong oxidants (e.g. superoxide radi cal, hydrogen peroxide and hydroxyl radical) called oxygen free radica ls or partially reduced forms of oxygen (PRFO). These highly reactive oxygen species can cause cellular injury by oxidizing lipids and prote ins as well as by causing strand breaks in nucleic acids. PRFO are pro duced in the cell during normal redox reactions including respiration and there are various antioxidants in the cell which scavenge these ra dicals. Thus in order to maintain a normal cell structure and function , a proper balance between free radical production and antioxidant lev els is absolutely essential. Production of PRFO in the myocardium is i ncreased during various in vivo as well as in vitro pathological condi tions and these toxic radicals are responsible for causing functional, biochemical and ultrastructural changes in cardiac myocytes. Indirect evidence of free radical involvement in myocardial injury is provided by studies in which protection against these alterations is seen in t he presence of exogenous administration of antioxidants. Endogenous my ocardial antioxidants have also been reported to change under various physiological as well as pathophysiological conditions. It appears tha t endogenous antioxidants respond and adjust to different stress condi tions and failure of these compensatory changes may also contribute in cardiac dysfunction. Thus endogenous and/or exogenous increase in ant ioxidants might have a therapeutic potential in various pathological c onditions which result from increased free radical production.