Oxidative stress is a contributing factor related to aging. Heretofore, the mechanism of action of antioxidants is one where the antioxidant supplies the free radicals that the electrons they need to stabilize them. Oxidative stress is used frequently to describe the toxic effects of free radicals and its contribution to the phenomenon of aging.
These could produce significant amounts of the superoxide free radical through normal metabolic pathways mediated by the enzyme superoxide dismutase (SOD). Recently with improved scientific progress and understanding, a far clearer picture is emerging. At the middle of the new understanding is a transcription factor called nuclear factor (erythroid-derived 2)-like 2, or Nrf2. High levels of free radicals turn on Nrf2 that is a protein that’s dormant until it’s triggered by a Nrf2 activator.
Once released Nrf2 migrates to the cell nucleus where it binds to the DNA in the location of the Antioxidant Response Element (ARE). The transcription factor Nrf2 binds to the ARE. Activation of the pathway drives expression of antioxidant enzymes. The mechanism of Nrf2 activation involves a protein called Keap1, a suppressor protein anchored in the cytoplasm that physically binds Nrf2. Activation of Nrf2 basically opens the door for the cell to generate a vast range of important antioxidants.
As it turns out many different foods such as turmeric, green tea extract in addition to coffee act are strong activators of the Nrf2 pathway. While not necessarily full of antioxidants in themselves, they directly empower and enhance the mobile’s innate ability to create vast antioxidant protection by signaling the DNA. This way, specific molecules out of Nrf2 triggering foods can trigger the creation of thousands of antioxidant molecules, providing better defense against the harmful effects of free radicals in contrast to standard antioxidant supplements.
Nrf2 fine-tunes the expression of numerous genes, including the familiar antioxidant enzymes along with a large numbers of genes that control apparently dissimilar processes like immune versus inflammatory reactions, tissue remodeling versus fibrosis, carcinogenesis versus metastasis, as well as cognitive dysfunction versus addictive behaviour. In effect the cells create their own antioxidants. Maybe all we have to do is help with phytonutrient Nrf2 activators. This idea becomes particularly attractive in light of the fact that Nrf2 expression seems to decline with aging, resulting in impairment of oxidative stress reactions.