Reactive oxygen species, produced by oxidative stress, are implicated in the initiation, promotion, and malignant conversion of carcinogenesis through activation/suppression of redox-sensitive transcription factors. NF-E2-related factor 2 (Nrf2) encodes for antioxidant and general cytoprotection genes, while NF-κB regulates the expression of pro-inflammatory genes. A variety of anti-inflammatory or anti-carcinogenic phyto-chemicals suppress NF-κB signalling and activate the Nrf2-ARE pathway. In this review we consider the role of Nrf2 and NF-κB in cancer pathogenesis and progression, focusing on their concerted modulation and potential cross-talk.

A procedure for 3,4‐dihydroxyphenylalanine decarboxylase from pig kidney purification is described in detail.The preparation has no detectable impurity on elecrophoresis and on ultracentrifugation and has a coenzyme content and a specific activity comparable with the same enzyme purified by other authors.However two significant differences are observed: a different stimulation of activity by added pyridoxal 5′‐phosphate and a nearly complete decarboxylation of L‐3,4‐dihydroxyphenylalanine in absence of added coenzyme.Absorption, fluorescence and circular dichroism properties of the coenzyme‐apoenzyme interaction are also described.The results are consistent with the existence of at least four coenzyme‐apoenzyme complexes, three of them active.