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Michael Jonathan Davies
Section of Cellular and Metabolic Research
Blegdamsvej 3, 2200 København N, 6.5
Prof. Michael Davies has pioneered studies on the formation and subsequent reactions of oxidants and other reactive species with proteins, DNA and carbohydrates, and the role of such reactions in biological damage.
He has made major contributions to the field of oxidants and oxidative damage. His work on protein modification and the detection and reactions of reactive intermediates is recognised nationally and internationally and has resulted in a number of significant awards and his election to a number of prestigious leadership positions in scientific societies.
He has held three prestigious fellowships from the Australian Research Council (QE2, Senior and Professorial), was Director of a (~25 million US$ per annum turnover) research institute, and led the Sydney (Australia) node of a highly-successful Australian Research Council Centre of Excellence in Free Radical Chemistry and Biotechnology (2006-2013) before moving to the University of Copenhagen, in 2014, after being awarded a Novo Nordisk Laureate research grant.
Primary fields of research
Protein oxidation has been detected at elevated levels on proteins present with human atherosclerotic lesions, the major underlying cause of most heart attacks and strokes. This damage is associated with increased morbidity and mortality, and has massive economic and social costs, but the processes that give rise to oxidation and the consequences of these reactions are poorly understood.
Prevention of oxidant damage in cardiovascular disease is in its infancy - many agents are being screened, but without adequate knowledge of the species involved and their reactions these efforts may not be well guided.
A key goal of our research is understanding the biochemical behaviour of oxidants associated with inflammation (e.g. hypochlorous acid, peroxynitrous acid, metal ions and radicals derived from these species) and elevated glucose levels (as seen in diabetes), and how these damage cells (endothelial, smooth muscle and macrophages) of relevance to cardiovascular disease, and their associated extracellular matrix.
These multidisciplinary projects are using a battery of tools including quantification of modified materials in human and animal tissues, cellular and animal studies, kinetic and mechanistic experiments, and computational chemistry. Such quantitative analysis is allowing the informed and rational development of novel preventive strategies.
Prof. Davies' research interests lie in the mechanisms of protein modification by reactive species (radicals, two-electron oxidants, glycation reactions), the biological consequences of such reactions, and the development of methods to quantify protein damage in disease with a particular emphasis on cardiovascular pathologies.
He also has interests in peroxidase enzymes (particularly myeloperoxidase), EPR spectroscopy for the detection of transient radicals, the kinetics of oxidant reactions, extracellular matrix damage and the development of antioxidants and inhibitors of oxidant formation.
- Oxidation- and glycation-induced changes in protein structure and function
- Extracellular matrix damage and atherosclerosis
- Kinetics and mechanisms of oxidative damage to proteins induced by hypochlorous acid, peroxynitrous acid, singlet oxygen, peroxides, sugars and metal ions
- Myeloperoxidase, inflammation and cardiovascular disease
- Novel selenium- and sulphur-based antioxidants
Fields of interest
Proteins are major targets for oxidation due to their abundance and rapid rates of reaction with oxidants. We want to understand in a quantitative and rigorous manner, the role of oxidants in protein damage, as such data will allow the rational and informed development of protective strategies against damage and disease.
A particular emphasis is being placed on protein oxidation and modification in cardiovascular disease, but the data obtained is also likely be of direct relevance to the pharmaceutical, food and hygiene industries, and agricultural production.