Influence of lipid peroxidation on β‐adrenoceptors

Abstract

The peroxidation of lipids in biological membranes is a destructive phenomenon that can be elicited in various ways. Surface receptor molecules that allow cells to respond to hormones are possibly inactivated during lipid peroxidation. Effects of lipid peroxidation on receptors have not been extensively examined thus far. This investigation shows that there is a decrease in β-adrenoceptor density (measured as specific (—)-[¹²⁵I]iodocyanopindolol binding) during lipid peroxidation, in both lungs and erythrocytes of the rat. To this end, lung membranes (containing both β₁- and β₂-adrenoceptors) and intact erythrocytes (containing a homogeneous β₂-adrenoceptor population) were pretreated with cumene hydroperoxide (lung membranes with 0.1 mM and erythrocytes with 1 mM) and Fe²⁺ (1 × 10⁻⁵ M) for 60 min which resulted in extensive lipid peroxidation measured as malondialdehyde formation. The ratio β₁-:β₂-adrenoceptor density in lung membranes after treatment with cumene hydroperoxide did not change and remained at 30%:70%. A single injection (i.p.) with the herbicide paraquat (50 , 24 h), which is known to cause lung damage via lipid peroxidation, resulted in similar alterations in receptor density to those caused by cumene hydroperoxide in the in vitro experiments.