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Population studies have shown a strong association between dietary intake of polyphenols and reduced risk of cardiovascular disease. These associations have been confirmed to some extent by intervention studies which have shown improvements in vascular function and blood pressure with certain polyphenols or food extracts rich in polyphenols. The mechanism involved in the bioactivity of dietary polyphenols is still under active investigation. It is unlikely that polyphenols act as antioxidants in vivo. Evidence suggests that dietary polyphenols or their metabolites act as signalling molecules and can increase nitric oxide bioavailability and induce protective enzymes. This talk will outline some of the evidence that dietary polyphenols regulate Hmox-1 and that this is critical for vascular protection by these compounds. The structural features of polyphenols such as flavonoids or their metabolites that are responsible for induction of Hmox-1 will be discussed. This research is providing mechanistic insights into the action of dietary bioactive compounds and expands our understanding of the role of food bioactives in improving health.

Aim Mouth rinses containing enzymes are designed for patients suffering from xerostomia. The objective of the present in situ study was to investigate the efficacy of these rinses for targeted accumulation and immobilisation of protective enzymes in the acquired pellicle. Methods A number of six healthy subjects carried bovine enamel slabs fixed on individual upper jaw splints for pellicle formation in situ. After 1 min, they rinsed with biotene or BioXtra for 10 min, respectively. Enzyme activities of lysozyme, peroxidase and glucoseoxidase in the in situ pellicle and in the saliva were assayed before as well as 0, 20 and 40 min after the rinses. The assays for the respective enzyme activities were based on fluorogenic substrates. Separate experiments were performed for the different enzymes and mouth rinses, respectively. Statistical evaluation was carried out with the Kruskal–Wallis test. Results None of the investigated rinses had any significant impact on the activities of lysozyme, peroxidase and glucoseoxidase detectable in the in situ pellicle or in the saliva (Kruskal–Wallis test, p > 0.05). Despite the fact that both products should contain lactoperoxidase activity according to manufacturers’ instructions, no peroxidase activity was measurable in the pure mouth rinses. Conclusion With the tested enzymatic mouth rinses targeted accumulation and immobilisation of protective enzymes in the in situ pellicle did not seem possible.

The aetiology of multiple sclerosis suggests that its occurrence depends on a combination of factors, including viral infection in early childhood, genotype and an initiating event within the central nervous system. The resulting damage may be caused by events initiated by free radicals. Free radicals themselves may cause damage to myelin and also may trigger the arachidonic acid cascade, to produce compounds that are thought to initiate and augment T-cell activity. Repair of the damaged tissue is normally achieved by protective enzymes that remove damaged lipid from the myelin.

Sulforaphane is a chemical found in cruciferous vegetables such as broccoli, sprouts and kale. This compound is a potent inducer of protective enzymes that provide defense against cancer-causing chemicals. Researchers have discovered that sulforaphane can halt human breast cancer cells in their tracks and have identified a new mechanism of action for the compound.

An extensive discussion is presented of the mechanisms of action of clinically useful anticancer agents in which free radical intermediates have been implicated in their cytotoxic action and/or metabolism. In addition the several factors contributing to drug metabolism and activation and interaction with macromolecular cell targets are discussed as they relate to free radical pathways. Consideration is also given to the action and levels in different tissues of cell protective enzymes against oxidative lesions and the clinicnal implication to anticancer drug action and toxicity.