Hydrogen peroxide is extensively used as a biocide, particularly in applications where its decomposition into non-toxic by-products is important. Although increasing information on the biocidal efficacy of hydrogen peroxide is available, there is still little understanding of its biocidal mechanisms of action. This review aims to combine past and novel evidence of interactions between hydrogen peroxide and the microbial cell and its components, while reflecting on alternative applications that make use of gaseous hydrogen peroxide. It is currently believed that the Fenton reaction leading to the production of free hydroxyl radicals is the basis of hydrogen peroxide action and evidence exists for this reaction leading to oxidation of DNA, proteins and membrane lipids in vivo. Investigations of DNA oxidation suggest that the oxidizing radical is the ferryl radical formed from DNA-associated iron, not hydroxyl. Investigations of protein oxidation suggest that selective oxidation of certain proteins might occur, and that vapour-phase hydrogen peroxide is a more potent oxidizer of protein than liquid-phase hydrogen peroxide. Few studies have investigated membrane damage by hydrogen peroxide, though it is suggested that this is important for the biocidal mechanism. No studies have investigated damage to microbial cell components under conditions commonly used for sterilization. Despite extensive studies of hydrogen peroxide toxicity, the mechanism of its action as a biocide requires further investigation.

Antimicrobials such as chlorine dioxide, peracetic acid and hydrogen peroxide (H₂O₂) share a basic mechanism of action (chemical oxidation of cellular components), but profound differences arise in their efficacy against microorganisms. Optimization of activity requires an understanding of their interaction with microbial targets and a clear differentiation between the chemical efficacies of each oxidative biocide. This study aimed to elucidate the biochemical mechanisms of action of oxidizing biocides at a macromolecular level, using amino acids, protein and an enzyme as model substrates for the action of each biocide. The interactions of a number of oxidising agents (liquid and gaseous H₂O₂, ClO₂, peracetic acid formulations) with amino acids, proteins (bovine serum albumin and aldolase) and enzymes were investigated by spectrophotometry, SDS-PAGE and alkaline phosphatase activity measurements. Biocide reactions yielded different types of oxidative structural change and different degrees of oxidation to amino acids and proteins, and differences in activity against a microbial enzyme. In particular there was a marked difference in the interactions of liquid H₂O₂ and gaseous H₂O₂ with the macromolecules, the latter causing greater oxidation; these results explain the dramatic differences in antimicrobial efficacy between liquid and gas peroxide. These results provide a comprehensive understanding of the differences in interactions between a number of oxidizing agents and macromolecules commonly found in microbial cells. Biochemical mechanistic differences between these oxidative biocides do exist and lead to differential effects on macromolecules. This in turn could provide an explanation as to their differences in biocidal activity, particularly between liquid and gas peroxide.

The study and synthesis of C-nucleosides has been extensive owing to their biological activity and potential as drug candidates for antiviral and anticancer therapy. Numerous synthetic strategies have also been investigated in order to optimize yields and stereoselectivity in the glycosylation reaction. Here we review one class of synthetic methods, direct condensation of a pre-formed aglycon unit with an appropriate sugar component.

Oestrogens and androgens stimulate growth in hormone-dependent breast and prostate cancers respectively. Modern strategies seek to remove the influence of hormones on tumour growth using anti-oestrogens (breast) or anti-androgens (prostate) which block the action of the hormone on its receptor. For prostate cancer patients LHRH (luteinising hormone releasing hormone) agonists, which decrease testes synthesis of testosterone are also used. Newer alternative (or sequential) strategies aim to deplete circulating and tissue levels of the respective mitogenic hormone by inhibition of a specific target enzyme involved in its steroidogenic pathway: for breast cancer - aromatase (P450AROM) or 17β-hydroxysteroid dehydrogenase (17β-HSD) Type 1 isoenzyme or the metabolic enzyme oestrogen sulfatase; for prostate cancer - 17α-hydroxylase: 17, 20-lyase (P450 17) or 5α-steroid reductase (5α-SR) or 17β-HSD Type 3 isoenzyme. The use of P450AROM inhibitors as sequential agents in breast cancer patients is well established;...