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Redox therapy is an experimental therapy [1] [2] that aims to effect an outcome by modifying the levels of pro-oxidant and antioxidant agents in cells. [3] The term "redox" is a contraction of "reduction-oxidation". For cancer patients, the therapy is predicated on the idea that the redox state of cells may have an effect on cancer development. [4]
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.
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]
Genetic activation of NRF2 may promote the development of de novo cancerous tumors [41] [42] as well as the development of atherosclerosis by raising plasma cholesterol levels and cholesterol content in the liver. [43] It has been suggested that the latter effect may overshadow the potential benefits of antioxidant induction afforded by NRF2 ...
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.
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.
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