A new generation of new superfoods that tackle heart disease and diabetes could be developed following research into a protein that helps keep cells in our bodies healthy. The beneficial substances comprise broccoli-derived sulforaphane and quercetin, which is found in high-levels in onions.
There is a longstanding principle that antioxidants reduce risk of certain pathological conditions, such as cancer, diabetes, atherosclerosis, aging, and neurodegeneration. Antioxidant supplements are popularly consumed and certain dietary choices are made with the belief that externally ramping up antioxidant capacity improves the ability to ward off potential oxidative damage caused by reactive oxygen species (ROS). Recent advances made in understanding redox homeostasis maintained via the Keap1/Nrf2 signaling pathway may challenge this concept of artificially supplying the body with antioxidants. The feedback nature of the redox system must be considered fully, as chronic ingestion of antioxidants may actually diminish the body’s endogenous, defensive antioxidant capability and could provide a favorable environment for pathological conditions to propagate.
The researchers, from the University's Warwick Medical School, successfully increased the speed of Nrf2's movement by artificially introducing health beneficial substances potential components of new superfoods.
The beneficial substances comprise broccoli-derived sulforaphane and quercetin, which is found in high-levels in onions.
The team used these insights to develop new food supplements, which are currently being trialled to decrease risk of developing diabetes and heart disease
Lead researcher Professor Paul Thornalley says, “The way Nrf2 works is very similar to sensors in electronic devices that rely on continual reassessment of their surroundings to provide an appropriate response”.
Discussing the health benefits of the research Professor Thornalley argues:
“The health benefit of Nrf2 oscillating at a fast speed is that surveillance of cell health is increased when most needed, that is, when cells are under threat. By understanding how this process works and increasing Nrf2's speed without putting cells under threat, new strategies for design of …
While supplementation with antioxidants is not altogether a bad idea, it’s interesting to consider the broader significance of “tweaking” the stress response pathway in the context of cancer. Increased antioxidant levels lower ROS and free radical levels in cells, eventually creating a reducing intracellular environment, keeping Keap 1 in a reduced configuration. With less oxidized Keap1 present, ubiquitination and degradation of Nrf2 increases, leading to a lower basal steady-state Nrf2 level and, subsequently, lower basal levels of endogenous antioxidant and phase II enzymes. If cancer cells have adapted this ROS stress-response pathway to their advantage, then disrupting redox and ROS homeostasis is a promising strategy to treat cancer with careful, targeted selection.
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