Free radical effects on myocardial membrane microviscosity.

Previous studies have shown that myocardial membranes, isolated from ischemic myocardial tissue, showed marked changes in microviscosity. To evaluate the contribution of free radical production and concomitant lipid peroxidation to these changes in microviscosity, the in vitro effects of two radical producing systems (H2O2/FeCl2 and xanthine oxidase/hypoxanthine/FeCl3) were investigated separately on the microviscosity of sarcolemmal, mitochondrial and sarcoplasmic reticulum membranes. In all three membranes both these free radical producing systems caused formation of malondialdehyde as quantitated by the thiobarbituric acid test. The sensitivity of the membranes to free radical damage differed: the sarcolemma was more sensitive to H2O2 damage, while mitochondrial malondialdehyde production was highest with xanthine oxidase. H2O2/FeCl2 caused a reduction in microviscosity (i.e. increased fluidity) of all three membranes, whereas the xanthine oxidase system increased mitochondrial and sarcolemmal microviscosity and reduced that of the sarcoplasmic reticulum. The similarity between ischemia-induced membrane microviscosity changes and those induced in vitro by xanthine oxidase, indicate a possible causal role for superoxide and hydroxyl free radicals produced during ischemia.