Background: A defective mucosal barrier function is the principal cause of the
uncontrolled onset and progression of a number of human inflammatory gut diseases, most of
which are characterized by chronic intermittent immune and inflammatory responses leading
to structural intestinal damage, which can represent a potential risk for colorectal cancer development.
During the active disease phase the production of pro-inflammatory cytokines and chemokines,
and the induction of oxidative reactions by activated leukocytes and epithelial cells represent
the main event in the intestinal inflammation.
Objective: Oxidative stress plays a key role in the development of intestinal damage. Indeed
reactive oxygen species and their oxidized by-products regulate redox-sensitive signaling
pathways and transcription factors, which sustain inflammation within the intestinal layer.
Methods: Polyunsaturated fatty acids and cholesterol are the principal targets of oxidative
These lipids, which are cell membrane constituents or are present in food, readily undergo
non-enzymatic oxidation to form chemically-reactive species that can induce a wide range of
biological effects including inflammation, programmed cell death, and proliferation.
Results and Conclusions: In this review we summarize the current knowledge on the role of
lipid oxidation products in regulating redox pathways involved in the pathogenesis of inflammation-
related gut diseases. In particular, lipid peroxidation end products, such as isoprostanes
and aldehydes, and cholesterol oxidation-derived oxysterols are taken into consideration.
The control of oxidative damage and consequently tissue local over-production of lipid oxidation
products by using specific antioxidant and anti-inflammatory molecules in the diet
may have clinical and therapeutic benefits.