Journal
NUTRIENTS
Volume 6, Issue 9, Pages 3777-3801Publisher
MDPI
DOI: 10.3390/nu6093777
Keywords
Nrf2; NF kappa B; Keap1; oxidative stress; glutathione; antioxidant enzymes; phase 2 enzymes; nutrient: gene interactions; phytochemicals; trace minerals; zinc; selenium
Categories
Funding
- AgriInnovation Program of Agriculture and Agri-Food Canada's Growing Forward 2 Policy Framework (a federal-provincial-territorial initiative)
- Organic Science Cluster II
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It has become increasingly evident that chronic inflammation underpins the development of many chronic diseases including cancer, cardiovascular disease and type 2 diabetes. Oxidative stress is inherently a biochemical dysregulation of the redox status of the intracellular environment, which under homeostatic conditions is a reducing environment, whereas inflammation is the biological response to oxidative stress in that the cell initiates the production of proteins, enzymes, and other compounds to restore homeostasis. At the center of the day-to-day biological response to oxidative stress is the Keap1/Nrf2/ARE pathway, which regulates the transcription of many antioxidant genes that preserve cellular homeostasis and detoxification genes that process and eliminate carcinogens and toxins before they can cause damage. The Keap1/Nrf2/ARE pathway plays a major role in health resilience and can be made more robust and responsive by certain dietary factors. Transient activation of Nrf2 by dietary electrophilic phytochemicals can upregulate antioxidant and chemopreventive enzymes in the absence of actual oxidative stress inducers. Priming the Keap1/Nrf2/ARE pathway by upregulating these enzymes prior to oxidative stress or xenobiotic encounter increases cellular fitness to respond more robustly to oxidative assaults without activating more intense inflammatory NFB-mediated responses.
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