Inflammatory bowel disease (IBD) comprises primarily the chronic relapsing inflammatory disorders, Crohn's disease and ulcerative colitis, with the former affecting any part of the gastrointestinal tract and the latter mainly afflicting the colon. The precise etiology of IBD remains unclear, and it is thought that interactions among various factors, including genetic factors, the host immune system and environmental factors, cause disruption of intestinal homeostasis, leading to dysregulated inflammatory responses of the gut. As inflammation is intimately related to formation of reactive intermediates, including reactive oxygen and nitrogen species (ROS/RNS), oxidative stress has been proposed as a mechanism underlying the pathophysiology of IBD. This review is intended to summarize succinctly recent new experimental and clinical evidence supporting oxidative stress as a pathophysiological component of IBD and point to the potential of using antioxidant compounds as promising therapeutic modalities of human IBD. The sources of ROS/RNS and the redox signaling mechanism underlying oxidative stress and inflammation in IBD are discussed to provide insight into the molecular basis of oxidative stress as a pathophysiological factor in IBD.

Alcoholic liver disease (ALD) is a major cause of morbidity and mortality worldwide. The spectrum of ALD ranges from fatty liver to alcoholic hepatitis and cirrhosis, which may eventually lead to the development of hepatocellular carcinoma. In developed countries as well as many developing nations, ALD is a major cause of end-stage liver disease that requires liver transplantation. The most effective therapy for ALD is alcohol abstinence; however, for individuals with severe forms of ALD and those in whom alcohol abstinence is not achievable, targeted therapies are absolutely necessary. In this context, advances of our understanding of the pathophysiology of ALD over the past two decades have contributed to the development of therapeutic modalities (e.g., pentoxifylline and corticosteroids) for the disease though the efficacy of the available treatments remains limited. This article is intended to succinctly review the recent experimental and clinical findings regarding the involvement of oxidative stress and redox signaling in the pathophysiology of ALD and the development of mechanistically-based antioxidant modalities to target the oxidative stress and redox signaling mechanisms of ALD. The biochemical and cellular sources of reactive oxygen and nitrogen species (ROS/RNS) and the dysregulated redox signaling pathways associated with alcohol consumption are particularly discussed to provide insight into the molecular basis of hepatic cell dysfunction and destruction as well as tissue remodeling underlying ALD.