Hepatic liver ischemia/reperfusion injury

Abstract

We thank Bhogal et al.1 for their comments on our review,1 and we shall address the points that they raised. Most aerobic cells will generate small amounts of reactive oxygen species (ROS) during normal cellular respiration, but these are effectively handled by the various cellular antioxidant systems to which we alluded in our review. Moreover, most aerobic cells will increase their rate of ROS generation during ischemia/reperfusion (IR).2 Hepatocytes are no exception and do increase their rate of ROS production after IR. Indeed, this is clearly demonstrated in Fig. 2 of our review. The more imperative issue is the relative contribution of IR-generated ROS from Kupffer cells, neutrophils, and hepatocytes to the induction and propagation of liver IR injury. As outlined in our review and by others,3 Kupffer cells and neutrophils are the main contributors to ROS generation after IR, with Kupffer cells making the greatest contribution to ROS generation in the early phase after reperfusion. Additionally, Bhogal et al.3 remarked that hepatocytes produce proinflammatory cytokines and chemokines after IR. The available evidence supports this as we have discussed in our review. Mahmoud Abu-Amara M.D* , Shiyu Yang Ph.D* , Niteen Tapuria M.S., F.R.C.S.* , Barry J. Fuller Ph.D* , Brian R. Davidson M.D., F.R.C.S.* , Alexander M. Seifalian Ph.D* , * Liver Transplantation and Hepatobiliary Unit, Royal Free Hospital, London, United Kingdom, Division of Surgery and Interventional Science, University College London, London, United Kingdom.