Oxygen free radicals and related “reactive oxygen species” (ROS) are fundamental to survival; they help drive evolution yet the damage that they can do (“oxidative damage”) is involved in most, if not all, human diseases and in ageing itself. My earliest contribution to this field was to elucidate the pathway used by plants to remove hydrogen peroxide (H2O2) (the ascorbate-glutathione cycle). Plants are key to human life; they supply us with oxygen, they provide a variety of nutrients with antioxidant abilities, and diets rich in plants lower the risk of developing many diseases, including diabetes, atherosclerosis, dementias and stroke. Exactly why is uncertain.
Despite the key role of oxidative damage, there has been a general lack of effectiveness of supplements of such “classical” antioxidants as ascorbate, vitamin E and β-carotene in decreasing risk or severity of human disease. There are multiple reasons for this, one being that these antioxidants are often ineffective in decreasing levels of oxidative damage in humans. They work better in cell culture and in rodent models (which questions the relevance of some rodent models of human disease, and cell culture studies can generate many artefacts). So how then can we minimize oxidative damage in the human body? Strategies will be discussed. Much of our research now focuses on ergothioneine, a diet-derived antioxidant that is avidly retained by the human body and particularly accumulated at sites of tissue injury, where it may help to diminish tissue damage. We have conducted a detailed study of how ergothioneine behaves when administered to humans or mice. Ergothioneine is made by fungi and some bacteria, although the list of those able to make it grows daily. Data on the relevance of ergothioneine to neurodegenerative diseases, and other conditions will be presented.
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