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Antioxidative stress is an overabundance of bioavailable antioxidant compounds that interfere with the immune system's ability to neutralize pathogenic threats. The fundamental opposite is oxidative stress, which can lead to such disease states as coronary heart disease or cancer.
The primary function of thioredoxin (Trx) is the reduction of oxidized cysteine residues and the cleavage of disulfide bonds. [10] Multiple in vitro substrates for thioredoxin have been identified, including ribonuclease, choriogonadotropins, coagulation factors, glucocorticoid receptor, and insulin.
The nutrient has been shown to help guard against breast cancer, while a diet rich in vitamin A has been linked to a lower risk for squamous cell carcinoma, a common form of skin cancer.
Antioxidants are helpful in reducing and preventing damage from free radical reactions because of their ability to donate electrons which neutralize the radical without forming another. Vitamin C, for example, can lose an electron to a free radical and remain stable itself by passing its unstable electron around the antioxidant molecule.
On the contrary, research indicates that although polyphenols are antioxidants in vitro, antioxidant effects in vivo are probably negligible or absent. [3] [4] [5] By non-antioxidant mechanisms still undefined, polyphenols may affect mechanisms of cardiovascular disease or cancer. [6]
NRF2 is a basic leucine zipper (bZIP) protein that may regulate the expression of antioxidant proteins that protect against oxidative damage triggered by injury and inflammation, according to preliminary research. [6] In vitro, NRF2 binds to antioxidant response elements (AREs) in the promoter regions of genes encoding cytoprotective proteins. [7]
Antioxidants is a peer-reviewed open-access scientific journal that covers various areas of antioxidants research, including biosynthesis, pharmacodynamics, and synthetic antioxidants. It is published by MDPI and was established in 2012. The editor-in-chief is Stanley Omaye (University of Nevada).
Oxidative stress mechanisms in tissue injury. Free radical toxicity induced by xenobiotics and the subsequent detoxification by cellular enzymes (termination).. Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. [1]