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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]
Small changes in cellular oxidant status can be sensed by specific proteins which regulate a set of genes encoding antioxidant enzymes. Such a global response induces an adaptive metabolism including ROS elimination, the bypass of injured pathways, reparation of oxidative damages and maintenance of reducing power.
The relative importance of the antioxidant and pro-oxidant activities of antioxidants is an area of current research, but vitamin C, which exerts its effects as a vitamin by oxidizing polypeptides, appears to have a mostly antioxidant action in the human body.
Lycopene is an antioxidant commonly found in tomatoes — it has been shown to prevent cell damage and provide myriad benefits to the body, including but not limited to helping improve sperm count.
NRF2 appears to participate in a complex regulatory network and performs a pleiotropic role in the regulation of metabolism, inflammation, autophagy, proteostasis, mitochondrial physiology, and immune responses. [10] Several drugs that stimulate the NFE2L2 pathway are being studied for treatment of diseases that are caused by oxidative stress ...
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.
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.
Cancer cells with elevated ROS levels depend heavily on the antioxidant defense system. ROS-elevating drugs further increase cellular ROS stress level, either by direct ROS-generation (e.g. motexafin gadolinium, elesclomol) or by agents that abrogate the inherent antioxidant system such as SOD inhibitor (e.g. ATN-224, 2-methoxyestradiol) and ...