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Inflammatory bowel disease (IBD) is characterised by an imbalance between pro-oxidant and anti-oxidant mechanisms. Cellular detoxification systems in IBD seem unable to adequately control the amplified generation of reactive oxygen species, put a stop to free radical injury and repair damaged cellular elements, suggesting that an increase in oxidative stress might be involved in the pathogenesis of IBD,1,2 although the underlying molecular mechanisms remain largely undefined. Human paraoxonase family members (PON1, PON2, PON3) possess anti-oxidant and anti-inflammatory properties.3–5 Despite the large impact of genetic variation on PON activity, its important role in controlling oxidative stress and inflammation,5–8 as well as its association with several pathophysiological conditions,4 no information is available on the relationship between PON genetic …
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