(1) Background:
Hyperglycemia leads to several biochemical and physiological consequences, such as the generation of
advanced glycation end products (AGEs) and
reactive oxygen species (ROS), which are involved in the development of several human diseases. Intestinal cells are continuously exposed to
pro-oxidants and lipid peroxidation products from ingested foods, and also to glyco-oxidative damage. It has been reported that
free radical generation may be linked to the development of
inflammation-related
gastrointestinal diseases. (2) Methods: The effects of high
glucose (HG) treatment (50 mM) were assessed in terms of
free radical production, lipid peroxidation, and AGEs formation. Furthermore, the expression and the antiapoptotic and
antioxidant activity of the
paraoxonase-2 (PON2)
enzyme in intestinal cells has been investigated. (3) Results: Caco-2 cells treated with media supplied with high
glucose (HG) (50 mM) showed, with respect to physiological
glucose concentration (25 mM), an increase in ROS production, lipid peroxidation, and AGEs formation. Moreover, a lower PON2 expression and activity in HG-treated cells was related to activation of the apoptotic pathways. (4) Conclusions: Our results demonstrated that high
glucose concentrations triggered glyco-oxidative stress in intestinal cells; the downregulation of PON2 could result in a higher oxidative stress and might contribute to intestinal dysfunction.