Free Radicals in Biology and Medicine: From Inflammation to Biotechnology

Oxidative stress and inflammatory cell death / tissue damage have been implicated in a wide array of human diseases, including cancer, neurodegenerative diseases, diabetes, inflammatory joint diseases, cardiovascular dysfunctions as well as ageing. Oxidative stress mediates the activation of transcription factors such as NFkB that, in turn, induce the transcription of certain genes promoting cytokine production. Release of these cytokines results in the enhancement of inflammatory responses and activation of endothelial cells in distant organs. The inflammatory cascade is then triggered by the induction of adhesion molecules and the generation of cytokines and other inflammatory mediators. Given that reactive oxygen and nitrogen species (ROS and RNS respectively) generated by infiltrated neutrophils into distant organs act directly as noxious agents reacting with molecular components, thereby enhancing inflammatory processes and therefore influencing cell viability, ROS and RNS have become potential therapeutic targets for prophylactic biofactors.
Whilst their production by phagocytic cells is, of course, essential for the eradication of invading pathogens, and the capacity of selected chemotherapeutic agents to generate such species in specific 'target' cells is well known in cancer research, the novel therapeutic actions and potential mechanisms of action of ozone as a microbicidal agent in clinical dentistry are now being advocated. The focus of this publication prominently encompasses the pivotal roles of ROS and RNS in the pathogenesis of many clinical conditions (together with their involvement in the ageing process of lower (yeast) cells, and higher organisms including plants), and discusses the potential applications of dietary-derived antioxidants to interfere with the biomolecular mechanisms of these processes and hence offer realistic therapeutic or prophylactic potentials.