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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]
Ferroptosis (also known as oxytosis) is a type of programmed cell death dependent on iron and characterized by the accumulation of lipid peroxides.Ferroptosis is biochemically, genetically, and morphologically distinct from other forms of regulated cell death such as apoptosis and necroptosis. [1]
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 ...
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.
Antioxidants play a crucial role in mitigating lipid peroxidation by neutralizing free radicals, thereby halting radical chain reactions. Key antioxidants include vitamin C and vitamin E . [ 8 ] Additionally, enzymes including superoxide dismutase , catalase , and peroxidase contribute to the oxidation response by reducing the presence of ...
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.
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]
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.