Abstract
The erythrocyte is a highly specialised cell with a limited metabolic repertoire. As an oxygen shuttle, it must continue to perform this essential task while exposed to a wide range of environments on each vascular circuit, and to a variety of xenobiotics across its lifetime. During this time, it must continuously ward off oxidant stress on the haeme iron, the globin chain and on other essential cellular molecules. Haemolysis, the acceleration of the normal turnover of senescent erythrocytes, follows severe and irreversible oxidant injury. A detailed understanding of the molecular mechanisms underlying oxidant injury and its reversal, and of the clinical and laboratory features of haemolysis is important to the medical toxicologist. This review will also briefly review glucose-6-phosphate deficiency, a common but heterogeneous range of enzyme-deficient states, which impairs the ability of the erythrocyte to respond to oxidant injury.