Inhibition of hepatocyte gap junctional communication by 25-hydroxycholesterol may be mediated through free radicals

Abstract

25-Hydroxycholesterol, an autoxidation product of cholesterol, has been shown to inhibit gap junctional communication between rat hepatocytes. In this study, we investigated whether free radicals are responsible for the effect of 25-hydroxycholesterol on hepatocytes. Addition of superoxide dismutase, hydroxyl radical scavenger mannitol, or the antioxidants diphenylphenylenediamine and α-tocopherol markedly decreased the inhibitory effect of 25-hydroxycholesterol. However, addition of catalase or the catalase inhibitor aminotriazole did not influence the inhibition of gap junctional communication by 25-hydroxycholesterol. Data from this study suggest that free radicals other than hydrogen peroxide are involved in the mechanism of 25-hydroxycholesterol-induced inhibition of gap junctional communication.