Oxygen-derived free radicals are produced when a period of intracellular anaerobic respiration is followed by re-oxygenation. These extremely reactive radicals combine with a large number of different protein and lipid molecules causing tissue damage and cell injury. The normal defences against such free radical attack include the presence in the tissues of antioxidant compounds and pathways of metabolism. A lack of sufficient antioxidant reserve during times of increased production of free radicals leads to the state of oxidative stress.

There has been increasing awareness over the last 20 years of the role played by oxidative stress in many inflammatory illnesses. Acute pancreatitis is no exception and in several models it has been demonstrated that oxygen-derived free radicals are generated during acute pancreatitis. It has been suggested that free radical generation, or the inability to quench free radicals, is an important factor in the pathogenesis of acute pancreatitis.¹ However, a careful experimental study suggested that oxidative stress alone cannot cause pancreatitis.² It is much more plausible that oxidative stress may contribute to worsening of the local inflammatory changes after onset of pancreatitis.^3–6 Some experimental studies suggest that antioxidant therapy can diminish tissue injury in acute pancreatitis.^3,7 It is also clear that oxidative mechanisms are an integral part of the inflammatory response and oxidative stress may contribute to pulmonary injury in severe acute pancreatitis.^8,9 Oxidative stress is recognised as part of the pathophysiology of adult respiratory distress syndrome,¹⁰ and there is experimental evidence that antioxidants can protect against …